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MicroRNA-206 suppresses hypoxia-inducible factor-1α/PFKFB3-mediated glycolysis to inhibit recurrence and metastasis of hepatocellular carcinoma after incomplete radiofrequency ablation 认领 引用
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作者 Dong Lu Li-Jun Wang +2 位作者 Jie Chai Jun Jiang Yan-Lin Tang 《World Journal of Gastrointestinal Oncology》 SCIE 2026年第4期232-243,共12页
BACKGROUND Hepatocellular carcinoma(HCC)remains one of the leading causes of cancer-related deaths,with high recurrence and metastasis rates after treatment.Incomplete radiofrequency ablation(iRFA)leaves residual tumo... BACKGROUND Hepatocellular carcinoma(HCC)remains one of the leading causes of cancer-related deaths,with high recurrence and metastasis rates after treatment.Incomplete radiofrequency ablation(iRFA)leaves residual tumor tissue that creates a hypoxic microenvironment that favors tumor progression.Emerging evidence suggests that microRNA-206(miR-206)may act as a tumor suppressor by regulating hypoxia-inducible factor-1α(HIF-1α)and its downstream glycolytic target 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3(PFKFB3).AIM To investigate whether miR-206 regulates the HIF-1α/PFKFB3/glycolysis axis in the recurrence and metastasis of HCC following iRFA.METHODS A clinical study was conducted in 45 patients with HCC undergoing RFA,comparing serum miR-206,HIF-1α,glucose,and pyruvate between complete(n=35)and incomplete ablation(n=10)groups.In vitro,tumor-derived endothelial cells(Td-ECs)exposed to sublethal thermal stress were evaluated for proliferation,migration,invasion,tube formation,and glycolysis after miR-206 mimic transfection or PFKFB3 knockdown.Dual-luciferase assays confirmed direct targeting of HIF-1αby miR-206.In vivo,a rabbit VX2 liver tumor model was used to compare angiogenesis,glycolysis,and molecular expression after complete or incomplete ablation.RESULTS Clinically,iRFA was associated with increased HIF-1αand pyruvate,decreased glucose,and altered miR-206 levels compared with complete ablation.In Td-ECs,thermal stimulation enhanced proliferation,migration,glycolysis,and HIF-1α/PFKFB3 expression,while miR-206 overexpression significantly attenuated these effects.Dual-luciferase assays confirmed that miR-206 directly binds the 3′UTR of HIF-1α.In animal models,incomplete ablation increased microvessel density,α-SMA,HIF-1α,and PFKFB3,while miR-206 expression was reduced.CONCLUSION miR-206 suppresses HIF-1α-driven PFKFB3-mediated glycolysis,thereby limiting angiogenesis,cell migration,and recurrence after iRFA.These findings suggest that miR-206 is a potential therapeutic target to reduce HCC recurrence and metastasis following ablation,although larger cohorts and in vivo rescue studies are warranted. 展开更多
关键词 MicroRNA-206 Hypoxia-inducible factor-1α 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 Glycolysis Incomplete radiofrequency ablation Hepatocellular carcinoma Tumor recurrence Angiogenesis
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Astrocyte glycolysis in Alzheimer’s disease:When the stars burn out 认领 引用
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作者 Simon M.Bell Heather Mortiboys 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第3期1130-1131,共2页
Alzheimer’s disease(AD)is the most common form of dementia characterized pathologically by the deposition of amyloid plaques and hyperphosphorylated tau containing neurofibrillary tangles.The disease presents clinica... Alzheimer’s disease(AD)is the most common form of dementia characterized pathologically by the deposition of amyloid plaques and hyperphosphorylated tau containing neurofibrillary tangles.The disease presents clinically with progressive memory loss and disruption of cognitive function.Currently,there is no cure for AD;recent advances in the therapeutics aimed at clearing the amyloid protein from the brain have led to potential disease stabilization,however,this does not prevent eventual disease progression(Cummings et al.,2024). 展开更多
关键词 hyperphosphorylated tau containing neurofibrillary tanglesthe memory loss alzheimer s disease ad Alzheimers disease astrocyte glycolysis amyloid protein amyloid plaques
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Comment on“α-hederin decreases the glycolysis level in intestinal epithelial cells via SNX10-mediated DEPDC5 degradation” 认领 引用
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作者 Haiping Hao 《Journal of Pharmaceutical Analysis》 SCIE CAS CSCD 2026年第1期3-4,共2页
Colorectal cancer(CRC)represents a global health challenge with significant societal burden,ranking among the most prevalent and lethal malignancies worldwide.Despite advances in understanding CRC pathogenesis,its mol... Colorectal cancer(CRC)represents a global health challenge with significant societal burden,ranking among the most prevalent and lethal malignancies worldwide.Despite advances in understanding CRC pathogenesis,its molecular mechanisms remain incompletely elucidated.Intestinal epithelial cells(IECs),the primary sites of CRC initiation,undergo genetic susceptibility alterations and mutations that drive carcinogenesis,highlighting the critical need to investigate IEC gene functions for identifying preventive targets. 展开更多
关键词 colorectal cancer crc represents intestinal epithelial cells epithelial cells iecs iec gene functions DEPDC alpha hederin glycolysis SNX
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Recycling of PVC tarpaulin reinforced with PET through glycolysis using betaine,a bio-based catalyst 认领 引用
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作者 Jae Kyun Kim Yejin Won +4 位作者 Jeonghoon Yoon Kyung Min Lee Yeyoon Choi Dong Hyun Kim Kyoung Heon Kim 《Chinese Journal of Catalysis》 SCIE EI CAS CSCD 2026年第2期366-379,共14页
Polyvinyl chloride(PVC)tarpaulins reinforced with poly(ethylene terephthalate)(PET)fibers are widely used in various industrial applications.However,the increasing demand for recycling PVC tarpaulin waste poses challe... Polyvinyl chloride(PVC)tarpaulins reinforced with poly(ethylene terephthalate)(PET)fibers are widely used in various industrial applications.However,the increasing demand for recycling PVC tarpaulin waste poses challenges because of the difficulty in separating the two different plastics.In this study,we investigated the possibility of recycling PVC and PET through the glycolysis of PET.The milled PVC tarpaulin underwent a glycolysis process,selectively depolymerizing the PET fibers into water-soluble bis(2-hydroxyethyl)terephthalate(BHET),while the PVC was removed by filtration.The PET fibers were selectively depolymerized by 77.6%after reacting at 190℃ for 2 h in the presence of 0.5%(w/w)betaine as a catalyst,quantitatively yielding BHET.During glycolysis,the physical appearance of the PVC changed because of leaching of the plasticizer,however,no dechlorination or shortening of the PVC polymer was observed.Interestingly,additives in PVC,such as CaCO3and CZ-stabilizer,act as catalysts for glycolysis,thereby enhancing PET depolymerization.The recovered PVC,when blended into a PVC formulation,maintained its mechanical properties and appearance up to 40 parts per hundred resins in roll-mill-processed sheets.In addition,ethylene glycol,which is used as a solvent in glycolysis,can be reused up to three times without the additional removal of BHET.This study demonstrated an industrially applicable method for simultaneously recycling PVC and PET from widely used tarpaulins. 展开更多
关键词 Plastic recycling Tarpaulin Polyvinyl chloride Poly(ethylene terephthalate) Glycolysis
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Isoliquiritigenin Impedes Breast Cancer Progression through PITX1-PFKP-Mediated Glycolysis Reprogramming 认领 引用
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作者 Cong Liu Zhenyu Zhang +6 位作者 Ronghua Feng Mengsi Zeng Hui Li Mei Zhu Lan Zhuang Zongjuan Li Tao Wu 《Oncology Research》 SCIE 2026年第5期825-845,共21页
Background:Breast cancer is the leading cause of cancer-related deaths in women,primarily due to distant metastasis.Metabolic reprogramming plays a critical role in tumor growth and spread,but the metabolic mechanisms... Background:Breast cancer is the leading cause of cancer-related deaths in women,primarily due to distant metastasis.Metabolic reprogramming plays a critical role in tumor growth and spread,but the metabolic mechanisms underlying metastasis in breast cancer remain unclear.The primary objective of this study is to identify molecular targets mediating breast cancer progression and to evaluate whether targeting the metabolic reprogramming represents a potential therapeutic strategy.Methods:To uncover key metabolic regulators involved in breast cancer progression,we analyzed high-throughput RNA sequencing data and identified Paired Like Homeodomain 1(PITX1)as a frequently upregulated oncogene.Its expression was further validated by immunohistochemistry,quantitative PCR,and western blotting across various metastatic breast cancer tissues.The correlation between PITX1 expression and patient survival was also evaluated.Functional assays were conducted to explore the role of PITX1 in promoting breast cancer proliferation and metastasis.As this study is primarily based on mechanistic cellular and bioinformatic analyses rather than clinical intervention trials,traditional clinical effect size metrics are not directly applicable.However,we have now ensured that all major findings include quantitative effect measurements(e.g.,fold changes,hazard ratios where applicable,correlation coefficients)together with corresponding statistical significance values to improve clarity and transparency.Results:Elevated PITX1 expression was significantly associated with poorer overall survival,distant metastasis-free survival,relapse-free survival,and post-progression survival in breast cancer patients.Silencing PITX1 significantly reduced breast cancer cell proliferation and suppressed glycolysis.Mechanistically,we found that PITX1 transcriptionally activates Phosphofructokinase platelet(PFKP),a key glycolytic enzyme,thereby enhancing glycolytic flux to promote tumor growth and metastatic capacity.Notably,isoliquiritigenin was identified as a small-molecule inhibitor that targets the PITX1-PFKP axis,downregulating glycolysis and consequently suppressing breast cancer progression.Conclusion:Our findings uncover a novel oncogenic mechanism by which PITX1 promotes breast cancer progression and metastasis through glycolytic reprogramming.Targeting the PITX1-PFKP axis with isoliquiritigenin offers a promising therapeutic strategy for breast cancer treatment. 展开更多
关键词 Breast cancer PITX1 PFKP metastasis glycolysis isoliquiritigenin
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Qianyang Yuyin granule(潜阳育阴颗粒)modulates glycolysis and inflammatory response to treat hypertensive cardiac remodeling 认领 引用
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作者 SUN Zeqi ZHANG Weiting +6 位作者 FAN Yadong XU Junyao HUANG Hong XIONG Ziwen CAO Huiting LIU Ming FANG Zhuyuan 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2026年第2期274-284,共11页
OBJECTIVE:To investigate the effect of Qianyang Yuyin granule(潜阳育阴颗粒QYYY)on Ang II-induced hypertensive cardiac remodeling,focusing on the role of pyruvate kinase isozyme M2(PKM2)mediated glycolysis.METHODS:A hy... OBJECTIVE:To investigate the effect of Qianyang Yuyin granule(潜阳育阴颗粒QYYY)on Ang II-induced hypertensive cardiac remodeling,focusing on the role of pyruvate kinase isozyme M2(PKM2)mediated glycolysis.METHODS:A hypertensive mouse model was established in male C57 BL/6 mice by continuous infusion of angiotensin II(AngII;1000 ng.kg-1.min-1).Mice were administered varying doses of QYYY,with sacubitril/valsartan(Sac/Val)serving as the positive control.Parameters evaluated included blood pressure,cardiac function,hypertrophy,fibrosis,inflammation,and apoptosis.The metabolic profile of myocardial tissue was analyzed using ultra performance liquid chromatography tandem mass spectrometry.Additionally,the involvement of the hypoxia-inducible factor 1-alpha(HIF-1α)/PKM2 signaling pathway was examined by Western blotting and immunohistochemistry.RESULTS:QYYY significantly lowered blood pressure,attenuated cardiac hypertrophy and fibrosis,reduced serum levels of inflammatory factors tumor necrosis factor-αand tumor necrosis factor-β,and decreased activation of phospho-NF-kappa B p65 pathway in cardiac tissue of hypertensive mice.Metabolomic analysis indicated that QYYY ameliorated cardiometabolic dysfunction,primarily associated with energy and amino acid metabolism,involving modulation of the HIF-1α/PKM2-mediated glycolytic pathway.CONCLUSION:QYYY effectively improves cardiac remodeling in hypertensive mice,potentially through inhibition of the PKM2-mediated glycolytic signaling pathway. 展开更多
关键词 cardiac remodeling glycolysis pyruvate kinase isozyme M2 Qianyang Yuyin granule
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Correction:miR-449a Suppresses LDHA-Mediated Glycolysis to Enhance the Sensitivity of Non-Small Cell Lung Cancer Cells to Ionizing Radiation 认领 引用
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作者 Liang Li Huijuan Liu +4 位作者 Lianjiang Du Pan Xi QianWang Yanqin Li Di Liu 《Oncology Research》 SCIE 2026年第7期737-738,共2页
In the article“miR-449a Suppresses LDHA-Mediated Glycolysis to Enhance the Sensitivity of Non-Small Cell Lung Cancer Cells to Ionizing Radiation”(Oncol Res,2018,Vol.26,No.4,pp.547–556.doi:10.3727/096504017X15016337... In the article“miR-449a Suppresses LDHA-Mediated Glycolysis to Enhance the Sensitivity of Non-Small Cell Lung Cancer Cells to Ionizing Radiation”(Oncol Res,2018,Vol.26,No.4,pp.547–556.doi:10.3727/096504017X15016337254605),an inadvertent error occurred during the compilation of Fig.3A and Fig.3C.This needed corrections to ensure the accuracy and integrity of the data presented. 展开更多
关键词 non small cell lung cancer ldha mir ionizing radiation glycolysis ionizing radiation oncol
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Modulating the Biological Processes and Glycolysis of Hepatocellular Carcinoma Cells by UBR7’s Suppression of Pyruvate Kinase PKM2 认领 引用
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作者 Bo Liu Xue Li 《BIOCELL》 SCIE 2026年第7期137-153,共17页
Background:As a key glycolytic enzyme,Pyruvate kinase M2(PKM2),which is highly expressed in cancer cells,promotes hepatocellular carcinoma(HCC)proliferation/metastasis.This research investigates the involvement of Ubi... Background:As a key glycolytic enzyme,Pyruvate kinase M2(PKM2),which is highly expressed in cancer cells,promotes hepatocellular carcinoma(HCC)proliferation/metastasis.This research investigates the involvement of Ubiquitin protein ligase E3 component N-recognin 7(UBR7)in HCC progression/glycolysis and its potential mechanisms.Methods:UBR7 expressions in HHL-5,Huh-7,and HepG2 cells were investigated using Quantitative Reverse Transcription Polymerase Chain Reaction andWestern Blot.Cell counting kit-8,clone formation experiment,scratch-wound assay,and transwell testing were conducted to assess the malignant biological behaviors of HepG2 and Huh-7 cells;the absorption level of glucose and generation levels of lactic acid and ATP were tested by assay kits.Huh-7 cells with stably overexpressed or knocked down UBR7 were inoculated into nude mice.Regular measurements were conducted on the tumor size,the tumors were isolated and weighed on the 35th day,and the glycolytic level in the tumor tissues was determined.Results:In HCC cells,UBR7 was significantly downregulated.Notably,UBR7 knockdown promoted HCC progression and glycolysis,increasing the viability of HepG2 and Huh-7 cells by 23%–24%(p<0.001),whereas UBR7 overexpression exerted the opposite inhibitory effects,resulting in a reduction of about 19%–31%in cell viability(p<0.001).UBR7 knockdown upregulated PKM2 expression in HCC cells,while UBR7 overexpression led to a marked reduction in PKM2 levels.Importantly,PKM2 overexpression partly abrogated the inhibitory impacts of UBR7 on HCC progression and glycolysis.In vivo experiments further demonstrated that UBR7 overexpression suppressed tumor growth and hindered glycolysis in nude mice.Conclusion:UBR7 suppressed PKM2 expression,thus hindering malignant biological progression and glycolysis in HCC,providing a potential therapeutic target for HCC treatment. 展开更多
关键词 Ubiquitin protein ligase E3 component N-recognin 7 pyruvate kinase M2 hepatocellular carcinoma glycolysis
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Construction of a Prognostic Model for Lung Adenocarcinoma Based on Bioinformatics Analysis of Glycolysis-Related Genes 认领 引用
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作者 Yongming Kang 《Proceedings of Anticancer Research》 2026年第2期1-10,共10页
Objective:This study aims to collect lung adenocarcinoma samples from the Cancer Genome Atlas(TCGA)database and explore the differential expression of glycolysis-related genes between lung adenocarcinoma tissues and a... Objective:This study aims to collect lung adenocarcinoma samples from the Cancer Genome Atlas(TCGA)database and explore the differential expression of glycolysis-related genes between lung adenocarcinoma tissues and adjacent normal tissues.By combining differentially expressed genes with prognostic data,we investigate the correlation between them and establish a prognostic prediction model for the survival rate of lung adenocarcinoma.Methods:Raw expression data were downloaded from the TCGA database and organized using the Perl language.Differential analysis was performed using the“limma”package in R software.Univariate Cox regression analysis was employed to screen glycolysis-related genes associated with the survival of lung adenocarcinoma patients.Correlation analysis and consensus clustering analysis were then conducted.Lasso regression analysis and 10-fold cross-validation were used to screen glycolysis-related genes associated with prognosis.Kaplan-Meier survival curves were plotted to confirm significant differences between high-and low-risk groups,and the receiver operating characteristic(ROC)curve was plotted to calculate the area under the curve(AUC).Finally,a risk model was constructed.Results:Based on data from the TCGA database,19 differentially expressed glycolysis-related genes were identified(17 upregulated and 2 downregulated).Univariate Cox regression analysis revealed that 14 genes were significantly associated with prognosis,among which five genes,including PGAM1 and NUP50,were identified as risk factors,while HK3 and PRKACA were protective factors.Following consensus clustering analysis,lung adenocarcinoma patients were classified into three subtypes.Survival analysis demonstrated significant prognostic differences among these subtypes,with subtype 2 exhibiting the worst prognosis.Using LASSO regression,11 key glycolysis-related genes were selected,and a risk scoring model was constructed based on these genes.According to this model,patients were divided into high-and low-risk groups,revealing significant differences in survival rates between the two groups(P<0.001).The ROC curve demonstrated the model’s good predictive ability for 1-,2-,and 3-year survival rates(AUCs of 0.742,0.725,and 0.673,respectively).Conclusion:This study found a correlation between glycolysis-related genes and the prognosis of lung adenocarcinoma.A risk scoring formula based on 11 key glycolysis-related genes was developed,and a risk model was constructed to predict the survival rate of lung adenocarcinoma patients using their risk scores along with T stage,N stage,and overall stage.This model provides valuable assistance for clinical research and individualized treatment of lung adenocarcinoma. 展开更多
关键词 Glycolysis Lung adenocarcinoma,TCGA database Prognostic model Bioinformatics
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Matrix stiffness regulates nucleus pulposus cell glycolysis by MRTF-A-dependent mechanotransduction 认领 引用 被引量：4
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作者 Haoran Xu Kang Wei +10 位作者 Jinhao Ni Xiaofeng Deng Yuexing Wang Taiyang Xiang Fanglong Song Qianliang Wang Yanping Niu Fengxian Jiang Jun Wang Lei Sheng Jun Dai 《Bone Research》 SCIE CAS CSCD 2025年第2期476-489,共14页
Increased matrix stiffness of nucleus pulposus(NP)tissue is a main feature of intervertebral disc degeneration(IVDD)and affects various functions of nucleus pulposus cells(NPCs).Glycolysis is the main energy source fo... Increased matrix stiffness of nucleus pulposus(NP)tissue is a main feature of intervertebral disc degeneration(IVDD)and affects various functions of nucleus pulposus cells(NPCs).Glycolysis is the main energy source for NPC survival,but the effects and underlying mechanisms of increased extracellular matrix(ECM)stiffness on NPC glycolysis remain unknown.In this study,hydrogels with different stiffness were established to mimic the mechanical environment of NPCs.Notably,increased matrix stiffness in degenerated NP tissues from IVDD patients was accompanied with impaired glycolysis,and NPCs cultured on rigid substrates exhibited a reduction in glycolysis. 展开更多
关键词 mechanotransduction nucleus pulposus cells npcs glycolysis increased matrix stiffness nucleus pulposus np tissue nucleus pulposus cells matrix stiffness intervertebral disc degeneration ivdd glycolysis
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Administration of Porphyromonas gingivalis in pregnant mice enhances glycolysis and histone lactylation/ADAM17 leading to cleft palate in offspring 认领 引用 被引量：2
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作者 Xige Zhao Xiaoyu Zheng +7 位作者 Yijia Wang Jing Chen Xiaotong Wang Xia Peng Dong Yuan Ying Liu Zhiwei Wang Juan Du 《International Journal of Oral Science》 SCIE CAS CSCD 2025年第2期268-284,共17页
Periodontal disease is a risk factor for many systemic diseases such as Alzheimer’s disease and adverse pregnancy outcomes.Cleft palate(CP),the most common congenital craniofacial defect,has a multifaceted etiology i... Periodontal disease is a risk factor for many systemic diseases such as Alzheimer’s disease and adverse pregnancy outcomes.Cleft palate(CP),the most common congenital craniofacial defect,has a multifaceted etiology influenced by complex genetic and environmental risk factors such as maternal bacterial or virus infection.A prior case-control study revealed a surprisingly strong association between maternal periodontal disease and CP in offspring.However,the precise relationship remains unclear.In this study,the relationship between maternal oral pathogen and CP in offspring was studied by sonicated P.gingivalis injected intravenously and orally into pregnant mice.We investigated an obvious increasing CP(12.5%)in sonicated P.gingivalis group which had inhibited osteogenesis in mesenchyme and blocked efferocytosis in epithelium.Then glycolysis and H4K12 lactylation(H4K12la)were detected to elevate in both mouse embryonic palatal mesenchyme(MEPM)cells and macrophages under P.gingivalis exposure which further promoted the transcription of metallopeptidase domain17(ADAM17),subsequently mediated the shedding of transforming growth factor-beta receptor 1(TGFBR1)in MEPM cells and mer tyrosine kinase(MerTK)in macrophages and resulted in the suppression of efferocytosis and osteogenesis in palate,eventually caused abnormalities in palate fusion and ossification.The abnormal efferocytosis also led to a predominance of M1 macrophages,which indirectly inhibited palatal osteogenesis via extracellular vesicles.Furthermore,pharmacological ADAM17 inhibition could ameliorate the abnormality of P.gingivalis-induced abnormal palate development.Therefore,our study extends the knowledge of how maternal oral pathogen affects fetal palate development and provides a novel perspective to understand the pathogenesis of CP. 展开更多
关键词 Pregnant Mice Sonicated Porphyromonas gingivalis Adam Cleft Palate congenital craniofacial defecthas Histone Lactylation periodontal disease Glycolysis
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Apatinib regulates the glycolysis of vascular endothelial cells through PI3K/AKT/PFKFB3 pathway in hepatocellular carcinoma 认领 引用 被引量：3
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作者 Yi Wu Bin-Bin Xie +3 位作者 Bing-Liang Zhang Qing-Xin Zhuang Shi-Wei Liu Hong-Ming Pan 《World Journal of Gastroenterology》 SCIE CAS 2025年第11期135-152,共18页
BACKGROUND Hepatocellular carcinoma(HCC)is a prevalent and aggressive malignancy in the Chinese population;the severe vascularization by the tumor makes it difficult to cure.The high incidence and poor survival rates ... BACKGROUND Hepatocellular carcinoma(HCC)is a prevalent and aggressive malignancy in the Chinese population;the severe vascularization by the tumor makes it difficult to cure.The high incidence and poor survival rates of this disease indicate the search for new therapeutic alternatives.Apatinib became a drug of choice because it inhibits tyrosine kinase activity,mainly through an effect on vascular endothelial growth factor receptor-2,thereby preventing tumor angiogenesis.This mecha-nism of action makes apatinib effective in the treatment of HCC.METHODS This present study has investigated the effects of HCC cells on VECs,paying particular attention to changes in the glycolytic activity of VECs.The co-culture system established in the present study examined key cellular functions such as extracellular acidification rate and oxygen consumption rate.It also discusses participation of apatinib in the above processes.Core to the findings is the phosphatidylinositol 3-kinase(PI3K)/AKT/6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3(PFKFB3)signaling pathway,emphasizing the function of phosphorylated AKT and its interaction with PFKFB3,an essential regulator of glycolysis.In the investigation,molecular mechanisms by which such a pathway could influence the above VECs functions of proliferation,migration,and tube formation were underlined through coimmunoprecipitation analysis.Besides,supplementary in vivo experiments on nude mice provided additional biological relevance to the obtained results.RESULTS The glycolytic metabolism in VECs co-cultured with HCC cells is highly active,and the increased glycolysis in these endothelial cells accelerates the malignant transformation of HCC cells.Apatinib has been shown to inhibit this glycolytic activity in the VECs.It also hinders the development,multiplication,and movement of these cells while encouraging their programmed cell death.Moreover,biological analysis revealed that apatinib mainly influences VECs by regulating the PI3K/AKT signaling pathway.Subsequent research indicated that apatinib blocks the PI3K/AKT/PFKEB3 pathway,which in turn reduces glycolysis in these cells.CONCLUSION Apatinib influences the glycolytic pathway in the VECs of HCC a through the PI3K/AKT/PFKFB3 signaling pathway. 展开更多
关键词 Apatinib Hepatocellular carcinoma Vascular endothelial cells Glycolysis Phosphatidylinositol 3-kinase Protein kinase B 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3
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Sirtuin 3 Attenuates Acute Lung Injury by Decreasing Ferroptosis and Inflammation through Inhibiting Aerobic Glycolysis 认领 引用 被引量：1
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作者 Kewei Qin Qingqing Ji +7 位作者 Weijun Luo Wenqian Li Bingbing Hao Haiyan Zheng Chaofeng Han Jian Lou Liming Zhao Xingying He 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2025年第9期1161-1167,共7页
Acute lung injury(ALI)/acute respiratory distress syndrome(ARDS)is a severe clinical disorder characterized by widespread inflammation,diffuse alveolar damage,and pulmonary edema,often leading to respiratory failure a... Acute lung injury(ALI)/acute respiratory distress syndrome(ARDS)is a severe clinical disorder characterized by widespread inflammation,diffuse alveolar damage,and pulmonary edema,often leading to respiratory failure and death.Despite significant advances in clinical care,ALI/ARDS remains the leading cause of death among intensive care unit patients.Sepsis is the primary risk factor for the development of ALI/ARDS,as excessive inflammatory responses contribute to organ injury and high mortality in critically ill patients. 展开更多
关键词 acute lung injury ali acute respiratory distress syndrome ards aerobic glycolysis severe clinical disorder intensive care ferroptosis inflammation sirtuin respiratory failure
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Acute hypoxia suppresses blood glycolysis in saker falcons(Falco cherrug)via NR3C1-mediated repression of HK1:Evidence from hematological and epigenomic profiling 认领 引用
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作者 Wei Wu Xiao-Hang Zhang +6 位作者 Fei-Fei Du Zhong-Ru Gu Li Hu Jun-Feng Chen Zhen-Zhen Lin Sheng-Kai Pan Xiang-Jiang Zhan 《Zoological Research》 SCIE CAS CSCD 2025年第5期1165-1174,共10页
Ongoing climate change is driving high-altitude bird species to occupy even higher elevations,yet physiological and regulatory responses enabling these transitions remain poorly understood.This study investigated acut... Ongoing climate change is driving high-altitude bird species to occupy even higher elevations,yet physiological and regulatory responses enabling these transitions remain poorly understood.This study investigated acute hypoxic responses in saker falcons(Falco cherrug)inhabiting the Qinghai-Xizang Plateau by exposing individuals to simulated altitudes of 5000-6000 m above sea level(a.s.l.),exceeding their typical elevation range(approximately 4300 m a.s.l.).GPS tracking data indicated that juvenile falcons maintained comparable activity levels across 4000-5000 m and 5000-6000 m a.s.l.ranges.However,pre-fledging individuals subjected to 6000 m hypoxia for three days exhibited marked increases in hemoglobin concentration and blood glucose.Transcriptomic profiling revealed significant suppression of glycolytic activity,notably characterized by reduced expression of hexokinase 1(HK1),a key enzymatic gene involved in the glycolytic pathway.ATAC-seq further identified enhanced chromatin accessibility within the HK1 locus under hypoxia,revealing two conserved cis-regulatory elements recognized by the transcription factor NR3C1 in the hypoxia-treated group.NR3C1 expression was negatively correlated with HK1.Notably,both elements were unique and evolutionarily conserved in avian taxa,suggesting a potential role in hypoxia resilience among highland birds.These findings provide mechanistic insights into the molecular and physiological strategies employed by sakers to tolerate acute hypoxic stress and inform conservation efforts for high-altitude bird species on the Qinghai-Xizang Plateau and other alpine ecosystems facing accelerating climate change. 展开更多
关键词 Hypoxic response Qinghai-Xizang Plateau Saker falcons Glycolysis Climate change
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Exploring the mechanism of Shenhua tablet(肾华片)alleviating renal injury by regulating macrophage glycolysis via hypoxia-inducible factor-1α/pyruvate kinase M2 signaling pathway in diabetic kidney disease mice 认领 引用
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作者 CHEN Yuanchun JING Jiaxing +5 位作者 LI Qingmin ZHOU Xiaohong JIN Xiaofei GAO Weijuan CHEN Xiangmei YU Wentao 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2025年第3期528-537,共10页
OBJECTIVE:To investigate the impact of Shenhua tablet(肾华片,SHT)on renal macrophage polarization and renal injury in mice with diabetic kidney disease(DKD)and to explore the potential mechanism involving the hypoxia-... OBJECTIVE:To investigate the impact of Shenhua tablet(肾华片,SHT)on renal macrophage polarization and renal injury in mice with diabetic kidney disease(DKD)and to explore the potential mechanism involving the hypoxia-inducible factor-1α(HIF-1α)and pyruvate kinase M2(PKM2)signaling pathway,along with the glycolysis metabolism pathway.METHODS:The animals were divided into the following groups:Model,Control,dapagliflozin,SHT low-dose,SHT medium-dose,and SHT high-dose.We assessed 24-hour urine protein(24 h-UTP)levels,urinary albuminto-creatinine ratio,and regularly monitored fasting blood glucose during the treatment period.After treatment,we examined renal tissue structure,renal function(urea nitrogen,uric acid,creatinine,cystatin C,β2-microglobulin),and glycolysis in renal macrophages.Additionally,we observed macrophage polarization in renal tissue and measured inflammatory factors(tumor necrosis factor-α,interleukin-1β,interleukin-6,interleukin-10,monocyte chemoattractant protein-1)to assess the immunoinflammatory status of the renal tissue.Finally,we investigated the expression of the HIF-1α/PKM2 signaling pathway in macrophages to explore its role in the glycolysis process.RESULTS:SHT shows a beneficial effect in treating DKD by reducing 24 h-UTP,regulating blood glucose levels,improving renal tissue structure,protecting renal function,inhibiting macrophage glycolysis,reducing macrophage transformation to the M1 state,and suppressing the expression of the HIF-1α/PKM2 signaling pathway.CONCLUSION:SHT may exert renoprotective effects by inhibiting macrophage glycolysis via the HIF-1α/PKM2 signaling pathway.This inhibition decreases macrophage M1 polarization and reduces immunoinflammatory injury in the renal tissue of DKD mice. 展开更多
关键词 diabetic kidney disease macrophages glycolysis hypoxia-inducible factor-1α pyruvate kinase M2 Shenhua tablet
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Inhibiting SHP2 reduces glycolysis, promotes microglial M1 polarization, and alleviates secondary inflammation following spinal cord injury in a mouse model 认领 引用 被引量：3
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作者 Xintian Ding Chun Chen +6 位作者 Heng Zhao Bin Dai Lei Ye Tao Song Shuai Huang Jia Wang Tao You 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第3期858-872,共15页
Reducing the secondary inflammatory response, which is partly mediated by microglia, is a key focus in the treatment of spinal cord injury. Src homology 2-containing protein tyrosine phosphatase 2(SHP2), encoded by PT... Reducing the secondary inflammatory response, which is partly mediated by microglia, is a key focus in the treatment of spinal cord injury. Src homology 2-containing protein tyrosine phosphatase 2(SHP2), encoded by PTPN11, is widely expressed in the human body and plays a role in inflammation through various mechanisms. Therefore, SHP2 is considered a potential target for the treatment of inflammation-related diseases. However, its role in secondary inflammation after spinal cord injury remains unclear. In this study, SHP2 was found to be abundantly expressed in microglia at the site of spinal cord injury. Inhibition of SHP2 expression using siRNA and SHP2 inhibitors attenuated the microglial inflammatory response in an in vitro lipopolysaccharide-induced model of inflammation. Notably, after treatment with SHP2 inhibitors, mice with spinal cord injury exhibited significantly improved hind limb locomotor function and reduced residual urine volume in the bladder. Subsequent in vitro experiments showed that, in microglia stimulated with lipopolysaccharide, inhibiting SHP2 expression promoted M2 polarization and inhibited M1 polarization. Finally, a co-culture experiment was conducted to assess the effect of microglia treated with SHP2 inhibitors on neuronal cells. The results demonstrated that inflammatory factors produced by microglia promoted neuronal apoptosis, while inhibiting SHP2 expression mitigated these effects. Collectively, our findings suggest that SHP2 enhances secondary inflammation and neuronal damage subsequent to spinal cord injury by modulating microglial phenotype. Therefore, inhibiting SHP2 alleviates the inflammatory response in mice with spinal cord injury and promotes functional recovery postinjury. 展开更多
关键词 apoptosis glycolysis inflammatory response microglia neurons polarization spinal cord injury Src homology 2-containing protein tyrosine phosphatase 2
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Andrographolide sulfonate alleviates rheumatoid arthritis by inhibiting glycolysis-mediated activation of PI3K/AKT to restrain Th17 cell differentiation 认领 引用 被引量：1
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作者 Chunhong Jiang Xi Zeng +8 位作者 Jia Wang Xiaoqian Wu Lijuan Song Ling Yang Ze Li Ning Xie Xiaomei Yuan Zhifeng Wei Yi Guan 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2025年第4期480-491,共12页
Andrographolide sulfonate(AS)is a sulfonated derivative of andrographolide extracted from Andrographis paniculata(Burm.f.)Nees,and has been approved for several decades in China.The present study aimed to investigate ... Andrographolide sulfonate(AS)is a sulfonated derivative of andrographolide extracted from Andrographis paniculata(Burm.f.)Nees,and has been approved for several decades in China.The present study aimed to investigate the novel therapeutic application and possible mechanisms of AS in the treatment of rheumatoid arthritis.Results indicated that administration of AS by injection or gavage significantly reduced the paw swelling,improved body weights,and attenuated pathological changes in joints of rats with adjuvant-induced arthritis.Additionally,the levels of tumor necrosis factor-alpha(TNF-α),interleukin-6(IL-6),and IL-1β in the serum and ankle joints were reduced.Bioinformatics analysis,along with the spleen index and measurements of IL-17 and IL-10 levels,suggested a potential relationship between AS and Th17 cells under arthritic conditions.In vitro,AS was shown to block Th17 cell differentiation,as evidenced by the reduced percentages of CD4+IL-17A+T cells and decreased expression levels of RORγt,IL-17A,IL-17F,IL-21,and IL-22,without affecting the cell viability and apoptosis.This effect was attributed to the limited glycolysis,as indicated by metabolomics analysis,reduced glucose uptake,and p H measurements.Further investigation revealed that AS might bind to hexokinase2(HK2)to down-regulate the protein levels of HK2 but not glyceraldehyde-3-phosphate dehydrogenase(GAPDH)or pyruvate kinase M2(PKM2),and overexpression of HK2 reversed the inhibition of AS on Th17 cell differentiation.Furthermore,AS impaired the activation of phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)signals in vivo and in vitro,which was abolished by the addition of lactate.In conclusion,AS significantly improved adjuvant-induced arthritis(AIA)in rats by inhibiting glycolysis-mediated activation of PI3K/AKT to restrain Th17 cell differentiation. 展开更多
关键词 Andrographolide sulfonate Rheumatoid arthritis Th17 cell differentiation Glycolysis PI3K/AKT pathway
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NAD+/SIRT1 pathway regulates glycolysis to promote oxaliplatin resistance in colorectal cancer 认领 引用 被引量：1
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作者 Ya-Ru Niu Mi-Dan Xiang +3 位作者 Wen-Wei Yang Yu-Ting Fang Hai-Li Qian Yong-Kun Sun 《World Journal of Gastroenterology》 SCIE CAS 2025年第11期118-134,共17页
BACKGROUND Glycolysis provides growth advantages and leads to drug resistance in colorectal cancer(CRC)cells.SIRT1,an NAD+-dependent deacetylase,regulates various cellular processes,and its upregulation results in ant... BACKGROUND Glycolysis provides growth advantages and leads to drug resistance in colorectal cancer(CRC)cells.SIRT1,an NAD+-dependent deacetylase,regulates various cellular processes,and its upregulation results in antitumor effects.This study investigated the role of SIRT1 in metabolic reprogramming and oxaliplatin resistance in CRC cells.AIM To investigate the role of SIRT1 in metabolic reprogramming and overcoming oxaliplatin resistance in CRC cells.METHODS We performed transcriptome sequencing of human CRC parental cells and oxaliplatin-resistant cells to identify differentially expressed genes.Key regulators were identified via the LINCS database.NAD+levels were measured by flow cytometry,and the effects of SIRT1 on oxaliplatin sensitivity were assessed by MTS assays,colony formation assays,and xenograft models.Glycolytic function was measured using Western blot and Seahorse assays.RESULTS Salermide,a SIRT1 inhibitor,was identified as a candidate compound that enhances oxaliplatin resistance.In oxaliplatin-resistant cells,SIRT1 was downregulated,whereasγH2AX and PARP were upregulated.PARP activation led to NAD+depletion and SIRT1 inhibition,which were reversed by PARP inhibitor treatment.The increase in SIRT1 expression overcame oxaliplatin resistance,and while SIRT1 inhibition increased glycolysis,the increase in SIRT1 inhibited glycolysis in resistant CRC cells,which was charac-terized by reduced expression of the glycolytic enzymes PKM2 and LDHA,as well as a decreased extracellular acidification rate.The PKM2 inhibitor shikonin inhibited glycolysis and reversed oxaliplatin resistance induced by SIRT1 inhibition.CONCLUSION SIRT1 expression is reduced in oxaliplatin-resistant CRC cells due to PARP activation,which in turn increases glycolysis.Restoring SIRT1 expression reverses oxaliplatin resistance in CRC cells,offering a promising therapeutic strategy to overcome drug resistance. 展开更多
关键词 Colorectal cancer Chemotherapy resistance Glycolysis SIRT1 NAD+
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STIL enhances the development of lung adenocarcinoma by regulating the glycolysis pathway 认领 引用 被引量：1
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作者 LEI WANG XIANJIN XIE 《Oncology Research》 SCIE 2025年第1期123-132,共10页
Background:To investigate SCL/TAL 1 interrupting locus(STIL)’s role and prognostic significance in lung adenocarcinoma(LUAD)progression,we examined STIL and E2 promoter binding factor 1(E2F1)expression and their impa... Background:To investigate SCL/TAL 1 interrupting locus(STIL)’s role and prognostic significance in lung adenocarcinoma(LUAD)progression,we examined STIL and E2 promoter binding factor 1(E2F1)expression and their impacts on LUAD prognosis using Gene Expression Profiling Interactive Analysis(GEPIA).Methods:Functional assays including CCK-8,wound-healing,5-ethynyl-2-deoxyuridine(EdU),Transwell assays,and flow cytometry,elucidated STIL and E2F1’s effects on cell viability,proliferation,apoptosis,and migration.Gene set enrichment analysis(GSEA)identified potential pathways,while metabolic assays assessed glucose metabolism.Results:Our findings reveal that STIL and E2F1 are overexpressed in LUAD,correlating with adverse outcomes.It enhances cell proliferation,migration,and invasion,and suppresses apoptosis,activating downstream of E2F1.Silencing E2F1 reversed the promotion effect of the STIL overexpression on cell viability and invasiveness.Importantly,STIL modulates glycolysis,influencing glucose consumption,lactate production,and energy balance in LUAD cells.Conclusion:Our model,incorporating STIL,age,and disease stage,robustly predicts patient prognosis,underscored STIL’s pivotal role in LUAD pathogenesis through metabolic reprogramming.This comprehensive approach not only confirms STIL’s prognostic value but also highlights its potential as a therapeutic target in LUAD. 展开更多
关键词 SCL/TAL1 interrupting locus(STIL) Lung adenocarcinoma E2 promoter binding factor 1 Glycolysis
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Emd-D inhibited ovarian cancer progression via PFKFB4-dependent glycolysis and apoptosis 认领 引用
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作者 Xin Zhao Chao Chen +7 位作者 Xuefei Feng Haoqi Lei Lingling Qi Hongxia Zhang Haiying Xu Jufeng Wan Yan Zhang Baofeng Yang 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2025年第4期431-442,共12页
Ovarian cancer poses a significant threat to women's health,necessitating effective therapeutic strategies.Emd-D,an emodin derivative,demonstrates enhanced pharmaceutical properties and bioavailability.In this stu... Ovarian cancer poses a significant threat to women's health,necessitating effective therapeutic strategies.Emd-D,an emodin derivative,demonstrates enhanced pharmaceutical properties and bioavailability.In this study,Cell Counting Kit 8(CCK8)assays and Ki-67 staining revealed dose-dependent inhibition of cell proliferation by Emd-D.Migration and invasion experiments confirmed its inhibitory effects on OVHM cells,while flow cytometry analysis demonstrated Emd-D-induced apoptosis.Mechanistic investigations elucidated that Emd-D functions as an inhibitor by directly binding to the glycolysis-related enzyme PFKFB4.This was corroborated by alterations in intracellular lactate and pyruvate levels,as well as glucose transporter 1(GLUT1)and hexokinase 2(HK2)expression.PFKFB4 overexpression experiments further supported the dependence of Emd-D on PFKFB4-mediated glycolysis and SRC3/mTORC1 pathway-associated apoptosis.In vivo experiments exhibited reduced xenograft tumor sizes upon Emd-D treatment,accompanied by suppressed glycolysis and increased expression of Bax/Bcl-2 apoptotic proteins within the tumors.In conclusion,our findings demonstrate Emd-D's potential as an anti-ovarian cancer agent through inhibition of the PFKFB4-dependent glycolysis pathway and induction of apoptosis.These results provide a foundation for further exploration of Emd-D as a promising drug candidate for ovarian cancer treatment. 展开更多
关键词 Ovarian cancer Emd-D Glycolysis Apoptosis PFKFB4
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