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Cell type-dependent role of transforming growth factor-βsignaling on postnatal neural stem cell proliferation and migration 认领 引用 被引量：1
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作者 Kierra Ware Joshua Peter +1 位作者 Lucas McClain Yu Luo 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第3期1151-1161,共11页
Adult neurogenesis continuously produces new neurons critical for cognitive plasticity in adult rodents.While it is known transforming growth factor-βsignaling is important in embryonic neurogenesis,its role in postn... Adult neurogenesis continuously produces new neurons critical for cognitive plasticity in adult rodents.While it is known transforming growth factor-βsignaling is important in embryonic neurogenesis,its role in postnatal neurogenesis remains unclear.In this study,to define the precise role of transforming growth factor-βsignaling in postnatal neurogenesis at distinct stages of the neurogenic cascade both in vitro and in vivo,we developed two novel inducible and cell type-specific mouse models to specifically silence transforming growth factor-βsignaling in neural stem cells in(mGFAPcre-ALK5fl/fl-Ai9)or immature neuroblasts in(DCXcreERT2-ALK5fl/fl-Ai9).Our data showed that exogenous transforming growth factor-βtreatment led to inhibition of the proliferation of primary neural stem cells while stimulating their migration.These effects were abolished in activin-like kinase 5(ALK5)knockout primary neural stem cells.Consistent with this,inhibition of transforming growth factor-βsignaling with SB-431542 in wild-type neural stem cells stimulated proliferation while inhibited the migration of neural stem cells.Interestingly,deletion of transforming growth factor-βreceptor in neural stem cells in vivo inhibited the migration of postnatal born neurons in mGFAPcre-ALK5fl/fl-Ai9 mice,while abolishment of transforming growth factor-βsignaling in immature neuroblasts in DCXcreERT2-ALK5fl/fl-Ai9 mice did not affect the migration of these cells in the hippocampus.In summary,our data supports a dual role of transforming growth factor-βsignaling in the proliferation and migration of neural stem cells in vitro.Moreover,our data provides novel insights on cell type-specific-dependent requirements of transforming growth factor-βsignaling on neural stem cell proliferation and migration in vivo. 展开更多
关键词 adult neurogenesis doublecortin hippocampus migration neural stem cells proliferation transforming growth factor-β
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A novel A-to-G mutation in circBDP1 alters adipocyte proliferation and differentiation and affects bovine carcass traits 认领 引用
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作者 Enhui JIANG Chiyuan ZHANG +7 位作者 Zhuoyuan HE Yuli ZHANG Yuta YANG Chuanying PAN Fugui JIANG Enliang SONG Sihuan ZHANG Xianyong LAN 《Journal of Zhejiang University-SCIENCE B》 SCIE CAS CSCD 2026年第8期918-922,I0024-I0032,共5页
Fat deposition in cattle,influenced by factors such as genetics,age,sex,and nutrition,plays a crucial role in determining growth rates,beef yield,and meat quality.Among these,genetics is the predominant factor(Kim et ... Fat deposition in cattle,influenced by factors such as genetics,age,sex,and nutrition,plays a crucial role in determining growth rates,beef yield,and meat quality.Among these,genetics is the predominant factor(Kim et al.,2020;Xing et al.,2025).Research in-dicates a high heritability for visceral(36%)and sub-cutaneous(57%)fat(Fox et al.,2012).Gene muta-tions that affect adipocyte function are significant con-tributors to variations in fat deposition and meat quality(Mannen,2011;Mwangi et al.,2019;Sun et al.,2023;Dementieva et al.,2024).Therefore,investigat-ing genetic variations in fat-related genes is essential for enhancing cattle performance. 展开更多
关键词 circbdp adipocyte function novel mutation carcass traits fat deposition adipocyte proliferation genetics adipocyte differentiation
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Lactate alleviates intestinal barrier injury in weaned piglets via activation of the Wnt/β-catenin pathway and promotion of intestinal epithelial cell proliferation 认领 引用
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作者 Mingyu Wang Yifan Chen +10 位作者 Jiaojiao Chen Aimin Wu Daiwen Chen Bing Yu Jun He Jie Yu Xiangbing Mao Zhiqing Huang Yuheng Luo Junqiu Luo Ping Zheng 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2026年第1期443-456,共14页
Background Inflammatory bowel disease causes intestinal structural damage,impairs gut function,hinders animal growth and development,and reduces farming efficiency.Previous studies demonstrated that lactate alleviates... Background Inflammatory bowel disease causes intestinal structural damage,impairs gut function,hinders animal growth and development,and reduces farming efficiency.Previous studies demonstrated that lactate alleviates dextran sulfate sodium(DSS)-induced inflammation and mitigates weight loss by enhancing intestinal barrier functions.However,the mechanisms underlying lactate-mediated protection of the intestinal epithelial barrier remain unclear.This study aimed to explore the protective effect of lactate on intestinal barrier damage in colitis piglets and the possible underlying mechanisms through in vivo and in vitro experiments.Methods A total of 6021-day-old weaned female piglets were randomly assigned into three groups based on weight:the control group(basal diet with physiological saline gavage),the DSS group(basal diet with 5%DSS gavage),and the DSS+LA group(2%lactate diet with 5%DSS gavage).There were 10 replicates per treatment,with 2 piglets per replicate.Jejunal morphology was assessed via hematoxylin and eosin staining,while Western blotting quantified the protein levels of proliferation markers,including cluster of differentiation 24(CD24),cyclin D1,and wingless/integrated(Wnt)/β-catenin signaling components.In vitro,0.08%DSS and 2–32 mmol/L sodium lactate-treated intestinal porcine epithelial cell line-J2(IPEC-J2)cells(n=4)were assessed for viability(Cell Counting Kit-8 assay),apoptosis(flow cytometry),and proliferation parameters,including cell cycle analysis and Leucine-rich repeat-containing G-protein coupled receptor 5(Lgr5+)stem cell quantification.Results In vivo,DSS administration induced jejunal villus shortening(P<0.05),downregulated protein levels of CD24,cyclin D1,casein kinase 1(CK1),and dishevelled-2(DVL2)(P<0.05).In vitro,DSS promoted apoptosis,inhibited proliferation,diminished the Lgr5+cell populations(P<0.05),and reduced S-phase cell proportions(P<0.05).Conversely,lactate supplementation ameliorated DSS-induced villus atrophy(P<0.05),restored CD24,cyclin D1,CK1,and DVL2 protein levels(P<0.05).Furthermore,in vitro,sodium lactate attenuated DSS-induced apoptosis(P<0.05),enhanced IPEC-J2 proliferation(P<0.05),expanded Lgr5+cells(P<0.05),and increased S-phase progression(P<0.05).Conclusions In summary,lactate ameliorated intestinal barrier damage in DSS-induced colitis by activating the Wnt/β-catenin pathway and restoring the balance between epithelial cell proliferation and apoptosis.This study provides novel mechanistic evidence supporting lactate's therapeutic potential for IBD management. 展开更多
关键词 Apoptosis Intestinal inflammation Lactate Lgr5 Piglets Proliferation Wnt/β-catenin pathway
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CDCA7 Promotes Proliferation and Suppresses Apoptosis in Gastric Cancer via HELLS-Mediated Chromatin Remodeling 认领 引用
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作者 Jun Jiang Yi-Ran Li +5 位作者 Xiaoting Wang Jian Li Fangzhou Ye Jiayi Wang Huanqing Li Li Feng 《Oncology Research》 SCIE 2026年第5期741-759,共19页
Background:In various tumor types,cell division cycle-associated 7(CDCA7)is involved in chromatin remodeling andDNA methylation.However,its biological functions and regulatorymechanisms in gastric cancer(GC)remain unk... Background:In various tumor types,cell division cycle-associated 7(CDCA7)is involved in chromatin remodeling andDNA methylation.However,its biological functions and regulatorymechanisms in gastric cancer(GC)remain unknown.This investigation intended to identify the function of CDCA7 in GC progression and elucidate its epigenetic regulatory mechanisms.Methods:Differentially expressed genes(DEGs)were detected fromthe GSE19826,TCGA-GC,and GSE56807 datasets.Networks of protein-protein interactions(PPI)and hub genes were discovered by the DMNC and Clustering Coefficient algorithms.Receiver operating characteristic(ROC)analysis and expression profiling were undertaken to determine diagnostic performance.In vitro assays,including CCK-8 assays,clonogenic assays,flow cytometry,dot blots,co-immunoprecipitation(Co-IP),chromatin immunoprecipitation(ChIP),and Western blots,were applied to evaluate the role of CDCA7 and its interaction with helicase,lymphoid-specific(HELLS).Results:169 overlapping genes were discovered,enriched in Cell adhesion molecules and ECM-receptor interaction.CDCA7 is highly expressed in GC and has high clinical diagnostic value.Knockdown of CDCA7 causes apoptosis and suppresses GC cell invasion,migration,and proliferation.Mechanistically,CDCA7 physically interacts with HELLS and promotes HELLS recruitment to chromatin.Knockdown of CDCA7 reduces global 5 hmC/5 mC levels and histone methylation(H3K9me3 and H4K20me3),while HELLS overexpression partially reverses these effects.Functionally,HELLS overexpression also partially reverses the antiproliferative and proapoptotic effects of CDCA7 knockdown.Conclusion:CDCA7 promotesGC progression by interactingwith HELLS to regulateDNAmethylation and chromatin stability,suggesting that the CDCA7-HELLS axis may serve as a potential diagnostic biomarker and therapeutic target for GC. 展开更多
关键词 CDCA7 HELLS chromatin remodeling gastric cancer proliferation apoptosis
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Regulation of Histone Emulsification by HPDL via LDHA/LDHB Promotes EC Cell Proliferation 认领 引用
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作者 Yan Wang Jialei Zhu +7 位作者 Shiyang Wei Lijie Jin Zhanqiu Liu Jie Xu Nana Yang Xuefeng Jiang Caizhi Wang Lingling Wang 《Oncology Research》 SCIE 2026年第5期711-740,共30页
Background:The role of 4-hydroxyphenylpyruvate dioxygenase-like protein(HPDL)in endometrial cancer(EC)progression remains poorly understood,particularly its involvement in metabolic-epigenetic crosstalk via lactate-dr... Background:The role of 4-hydroxyphenylpyruvate dioxygenase-like protein(HPDL)in endometrial cancer(EC)progression remains poorly understood,particularly its involvement in metabolic-epigenetic crosstalk via lactate-driven histone lactylation.This study aimed to investigateHPDL’smechanistic contribution to EC pathogenesis.Methods:Stable HPDL-overexpressing and knockdown EC cell lines(HEC-1-B and AN3CA)were generated using lentiviral vectors.Functional assays(proliferation,migration,invasion),subcutaneous xenograft models in BALB/c nude mice,and molecular analyses were conducted.Lactate levels,Pan-lysine lactylation(pan-kla),histone H3K18 lactylation(H3K18la),and effects of sodium oxamate(lactate modulator)were assessed.Lactate Dehydrogenase A/Lactate Dehydrogenase B(LDHA/LDHB)knockdown,promoter activity assays,and chromatin immunoprecipitation(ChIP)were performed to evaluate H3K18la occupancy at LDHA/LDHB promoters.Results:HPDL knockdown reduced intracellular lactate,Pan-Kla,and H3K18la levels,while overexpression elevated these markers.Sodium oxamate amplified lactate and lactylation in HPDL-overexpressing cells but suppressed histone lactylation independently of HPDL.LDHA/LDHB knockdown diminished lactylation,repressed HPDL expression,and inhibited promoter activity.ChIP revealed H3K18la enrichment at LDHA/LDHB promoters in HPDL-overexpressing cells and reduced occupancy in knockdown models.HPDL enhanced EC cell proliferation,migration,and invasion in vitro.In vivo,HPDLoverexpressing xenografts exhibited accelerated tumor growth and larger volumes compared to controls.Conclusions:HPDL regulates histone lactylation via LDHA/LDHB and promotes the proliferation of EC cells. 展开更多
关键词 Endometrial cancer histone lactylation 4-hydroxyphenylpyruvate dioxygenase-like protein lactate dehydrogenase A/B cell proliferation
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Small extracellular vesicles derived from hair follicle neural crest stem cells enhance perineurial cell proliferation and migration via the TGF-β/SMAD/HAS2 pathway 认领 引用
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作者 Yiming Huo Bing Xiao +8 位作者 Haojie Yu Yang Xu Jiachen Zheng Chao Huang Ling Wang Haiyan Lin Jiajun Xu Pengfei Yang Fang Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第5期2060-2072,共13页
Peripheral nerve defect repair is a complex process that involves multiple cell types;perineurial cells play a pivotal role.Hair follicle neural crest stem cells promote perineurial cell proliferation and migration vi... Peripheral nerve defect repair is a complex process that involves multiple cell types;perineurial cells play a pivotal role.Hair follicle neural crest stem cells promote perineurial cell proliferation and migration via paracrine signaling;however,their clinical applications are limited by potential risks such as tumorigenesis and xenogeneic immune rejection,which are similar to the risks associated with other stem cell transplantations.The present study therefore focuses on small extracellular vesicles derived from hair follicle neural crest stem cells,which preserve the bioactive properties of the parent cells while avoiding the transplantation-associated risks.In vitro,small extracellular vesicles derived from hair follicle neural crest stem cells significantly enhanced the proliferation,migration,tube formation,and barrier function of perineurial cells,and subsequently upregulated the expression of tight junction proteins.Furthermore,in a rat model of sciatic nerve defects bridged with silicon tubes,treatment with small extracellular vesicles derived from hair follicle neural crest stem cells resulted in higher tight junction protein expression in perineurial cells,thus facilitating neural tissue regeneration.At 10 weeks post-surgery,rats treated with small extracellular vesicles derived from hair follicle neural crest stem cells exhibited improved nerve function recovery and reduced muscle atrophy.Transcriptomic and micro RNA analyses revealed that small extracellular vesicles derived from hair follicle neural crest stem cells deliver mi R-21-5p,which inhibits mothers against decapentaplegic homolog 7 expression,thereby activating the transforming growth factor-β/mothers against decapentaplegic homolog signaling pathway and upregulating hyaluronan synthase 2 expression,and further enhancing tight junction protein expression.Together,our findings indicate that small extracellular vesicles derived from hair follicle neural crest stem cells promote the proliferation,migration,and tight junction protein formation of perineurial cells.These results provide new insights into peripheral nerve regeneration from the perspective of perineurial cells,and present a novel approach for the clinical treatment of peripheral nerve defects. 展开更多
关键词 hair follicle neural crest stem cells HAS2 migration miR-21-5p perineurial cells proliferation peripheral nerve injury Smad7 small extracellular vesicles transforming growth factor-β/SMAD signaling pathway
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Comprehensive Bioinformatics Analysis and Experimental Verification RNF186 Is a Recurrence Signature Gene of Hepatocellular Carcinoma that Promotes Cell Proliferation 认领 引用
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作者 Shanbao Ke Junya Yan +1 位作者 Xiao Feng Baiyu Li 《Oncology Research》 SCIE 2026年第4期705-735,共31页
Objectives:Tumor recurrence is a major determinant of poor prognosis in hepatocellular carcinoma(HCC),yet its cellular and molecular basis remains incompletely understood.This study aimed to identify recurrenceassocia... Objectives:Tumor recurrence is a major determinant of poor prognosis in hepatocellular carcinoma(HCC),yet its cellular and molecular basis remains incompletely understood.This study aimed to identify recurrenceassociated genes at single-cell resolution and to develop a prognostic model for predicting survival outcomes and immunotherapy responsiveness in HCC.Methods:Single-cell RNA sequencing data from 12 primary and 6 recurrent HCC samples were integrated and analyzed to identify genes characteristic of recurrence.After quality control,principal component analysis,and t-SNE-based clustering were used to identify highly variable genes for cell clustering and annotation.Based on macrophage characteristic genes,a recurrence-related risk score was constructed using a LASSOCox regression model,and a nomogram integrating clinical variables was developed.Prognostic performance was assessed using Kaplan-Meier analysis and time-dependent ROC curves.Immune infiltration profiling was performed to compare immune characteristics between risk groups defined by the prognostic model.Multivariate Cox regression was applied to identify independent prognostic biomarkers,which were subsequently validated by cell function experiments.Results:The risk model effectively stratified patients into high-and low-risk groups with distinct survival outcomes,demonstrating high predictive accuracy for 1-,3-,and 5-year survival.High-risk patients showed altered immune profiles and a reduced predicted response to immunotherapy.GRID2,RNF186,and SLC4A10 were identified as independent prognostic genes,with RNF186 promoting HCC cell proliferation in a SESN2-dependent manner.Conclusion:This prognostic model provides new insights into precision medicine and immunotherapy for HCC,highlighting the potential clinical significance of RNF186 as a therapeutic target. 展开更多
关键词 Hepatocellular carcinoma single-cell RNA sequencing recurrence RNF186 cell proliferation
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Novel Small Molecule DZ-865B Effectively Degrades BCL6,Promotes Apoptosis and Reduces Proliferation of Diffuse Large B-Cell Lymphoma Cells 认领 引用
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作者 Yanfeng Wang Xinyi Chen +2 位作者 Yichen Yin Tao Li Jing Chen 《Oncology Research》 SCIE 2026年第3期602-621,共20页
Objectives:B-cell lymphoma 6(BCL6)is a transcriptional repressor whose overexpression is closely linked to the progression of diffuse large B-cell lymphoma(DLBCL),making it a promising therapeutic target.This study ai... Objectives:B-cell lymphoma 6(BCL6)is a transcriptional repressor whose overexpression is closely linked to the progression of diffuse large B-cell lymphoma(DLBCL),making it a promising therapeutic target.This study aims to identify a novel small molecule,synthesized via proteolysis-targeting chimeras(PROTACs),capable of degrading BCL6,thereby inhibiting DLBCL growth and providing a foundation for future preclinical studies.Methods:The expression of BCL6 in DLBCL was analyzed using The Cancer Genome Atlas(TCGA)database and the Human Protein Atlas.Western blotting assays confirmed BCL6 expression in tumor cell lines,leading to the identification of the small molecule compound DZ-865B.To evaluate DZ-865B’s in vitro efficacy,multiple assays were performed,including protein immunoblotting,immunofluorescence,reverse transcription quantitative PCR,EDU proliferation,and soft agar cloning assays.Results:TCGA analysis revealed significant overexpression of BCL6 in DLBCL(p<0.05),corroborated by immunohistological staining and western blotting.DZ-865B induced BCL6 degradation in DLBCL cell lines(OCI-LY-1 and SU-DHL-4)in a concentration-and time-dependent manner,and induced the degradation of nuclear BCL6 through the ubiquitin-proteasome pathway.Notably,DZ-865B did not alter BCL6 mRNA levels but modulated downstream gene expression,leading to the activation of apoptosis pathway proteins and inhibition of DNA synthesis,effectively suppressing DLBCL cell growth.Conclusion:This study demonstrates that the small molecule DZ-865B targets and degrades BCL6 in DLBCL cells,promoting apoptosis and inhibiting cellular proliferation.These findings highlight DZ-865B as a potential therapeutic agent for diffuse large B-cell lymphoma. 展开更多
关键词 Diffuse large B-cell lymphoma(DLBCL) B-cell lymphoma 6(BCL6) proteolysis-targeting chimeras(PROTACs) proliferation
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Myostatin promotes proliferation of bovine muscle satellite cells through activating TRPC4/Ca2+/calcineurin/NFATc3 pathway 认领 引用 被引量：1
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作者 Yajie Gao Song Wang +12 位作者 Anqi Di Chao Hai Di Wu Zhenting Hao Lige Bu Xuefei Liu Chunling Bai Guanghua Su Lishuang Song Zhuying Wei Zhonghua Liu Lei Yang Guangpeng Li 《Journal of Integrative Agriculture》 SCIE CAS CSCD 2026年第3期1125-1136,共12页
Myostatin(MSTN)is principally expressed in skeletal muscle and negatively regulates muscle growth and development.MSTN mutation can induce muscle overgrowth in cattle by activating cell proliferation,presenting a“dou... Myostatin(MSTN)is principally expressed in skeletal muscle and negatively regulates muscle growth and development.MSTN mutation can induce muscle overgrowth in cattle by activating cell proliferation,presenting a“double-muscle”phenotype.However,the specific regulatory mechanism is still unclear.Here,we found that Ca2+content in muscle tissue and muscle satellite cells of MSTN mutated(MSTN–/–)cattle were significantly increased compared to wild-type(WT).Furthermore,transcriptome analysis of muscle satellite cells revealed that TRPC4 was significantly increased in MSTN–/–cattle.And the expression of TRPC4 in muscle tissue of MSTN–/–cattle was detected by RT-qPCR and Western blot,which was significantly higher than that of WT.These results suggested that MSTN mutation promoted muscle satellite cells proliferation through activation of TRPC4 channel.To further verify,ML204,a specific inhibitor of TRPC4,was used to treat MSTN–/–muscle satellite cells.We found that cell proliferation was inhibited,calcineurin expression was downregulated,and the entry of NFATc3 into nuclei was reduced,which was similar to WT group.Thus,MSTN mutation leads to the activation of TRPC4 channel,which increases intracellular Ca2+content,further activates calcineurin/NFATc3 pathway,and ultimately promotes the proliferation of muscle satellite cells. 展开更多
关键词 myostatin cell proliferation Ca2+ TRPC4 NFATc3
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Kynurenine promotes porcine intestinal epithelial cell proliferation by activating the AHR-MST1-YAP1 axis 认领 引用
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作者 Zhenguo Hu Lanmei Yin +6 位作者 Qianqian Wang Junhao Deng Xiaofeng Zhu Huansheng Yang Pengpeng Zhang Yulong Yin Xiongzhuo Tang 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2026年第3期1591-1608,共18页
Background The objective of this study was to investigate the effect of L-tryptophan(L-Trp)and its metabolite kynurenine(Kyn)on the regulation of porcine intestinal epithelial cell proliferation.Results Dietary supple... Background The objective of this study was to investigate the effect of L-tryptophan(L-Trp)and its metabolite kynurenine(Kyn)on the regulation of porcine intestinal epithelial cell proliferation.Results Dietary supplementation of L-Trp significantly increased villus height and decreased crypt depth in the jejunum and ileum of weaned pigs.mRNA sequencing data and qPCR analysis found that L-Trp activated the expression of cell proliferative genes and the AHR(aryl hydrocarbon receptor)-MST1(mammalian STE20-like kinase 1)-YAP1(Yesassociated protein 1)axis in the ileum.Further in vitro analysis revealed that L-Trp treatment significantly enhanced cell proliferation of intestinal porcine epithelial cells-jejunum 2(IPEC-J2)cells by activating the MST1-YAP1 signaling pathway.Further targeted metabolomics analysis identified Kyn as the core Trp metabolite involved in promoting IPEC-J2 cell proliferation.Mechanistically,Kyn interacted with AHR,which in turn bound to the upstream promote region of MST1 to initiate the transcription of downstream target gene YAP1 to activate intestinal epithelial cell proliferation.Furthermore,porcine intestinal organoid model also demonstrated that Kyn promoted intestinal organoidbudding efficiency and intestinal stem cell proliferation.Importantly,by using the AHR-or YAP1-specific inhibitors,the data confirmed that the Kyn-induced intestinal epithelial cell proliferation in IPEC-J2 cells and intestinal organoids was dependent on the activation of the AHR-MST1-YAP1 axis.Conclusions Together,this study has revealed a regulatory mechanism of Trp metabolism-derived Kyn in promoting porcine intestinal epithelial cell proliferation,offering insights into the connection between nutrient metabolism and intestinal epithelial homeostasis. 展开更多
关键词 Aryl hydrocarbon receptor Intestinal epithelial cell proliferation Kynurenine Tryptophan metabolism
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Cell proliferation and differentiation during epidermis renewal 认领 引用
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作者 Kai LIU Kaidi REN +1 位作者 Dengwen LI Yang YANG 《Journal of Zhejiang University-SCIENCE B》 SCIE CAS CSCD 2026年第6期603-614,I0014,共12页
Residing at the outermost layer of the skin,the epidermis is composed of stratified squamous epithelial cells.Regular renewal of the epidermis is essential for maintaining its barrier function,which is dependent on th... Residing at the outermost layer of the skin,the epidermis is composed of stratified squamous epithelial cells.Regular renewal of the epidermis is essential for maintaining its barrier function,which is dependent on the orchestrated proliferation and differentiation of stem cells located in the basal epidermis.This process necessitates precise dual regulation through the intrinsic control of cell division orientation and external microenvironmental influences.In this comprehensive review,we delve into the critical processes underlying epidermis renewal,emphasizing the balance between symmetric and asymmetric cell fate and the integration of differentiated cells into the suprabasal layer.Our paper highlights the pivotal roles of single-cell omics,live imaging,and artificial intelligence(AI)-driven modeling techniques in elucidating the molecular mechanisms governing cell proliferation and differentiation during epidermis renewal. 展开更多
关键词 Epidermis renewal Stem cell proliferation Asymmetric cell division Basement membrane dynamics Single-cell omics Mechanotransduction
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Lithospermic Acid Promotes Osteoblast Proliferation and Differentiation through the Wnt/β-Catenin Signaling Pathway 认领 引用
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作者 Jianfeng Wang Zhongqing Hu +5 位作者 Jiandong Guo Xin Jin Lei Cai Jian Li Jinxi Zhang Dongan He 《BIOCELL》 SCIE 2026年第2期128-147,共20页
Objectives Therapeutic strategies for enhancing bone regeneration and combating osteoporosis remain a significant unmet medical need.This study aims to elucidate Lithospermic acid(LA)’s regulatory effects on osteobla... Objectives Therapeutic strategies for enhancing bone regeneration and combating osteoporosis remain a significant unmet medical need.This study aims to elucidate Lithospermic acid(LA)’s regulatory effects on osteoblast proliferation and differentiation,investigating its viability as a bone-healing agent.Methods This study employed various cellular and molecular biology experiments to assess the effects of LA on the viability,proliferation,cell cycle,apoptosis,differentiation,mineralization,and migration of MC3T3-E1 osteoblasts.Immunofluorescence and Western blot analyses were conducted to detect the expression of proteins related to the Wnt/β-catenin signaling pathway,investigating the regulatory mechanisms by which LA promotes osteoblast proliferation and differentiation.Additionally,Wnt inhibitor dickkopf-1(DKK-1)andβ-catenin-silenced cell models were used to further validate the role of LA in modulating this signaling pathway.Results LA significantly promoted osteoblast proliferation without apparent cytotoxicity.Flow cytometry showed that LA regulated the cell cycle by reducing G0/G1 phase arrest and promoting G2/M phase progression.Western blot results indicated that LA upregulated the expression of proteins associated with cell proliferation and enhanced osteoblast differentiation and mineralization.Immunofluorescence and Western blot analyses further confirmed that LA markedly increased the expression of Wnt andβ-catenin,facilitatingβ-catenin nuclear translocation.Treatment with the DKK-1 inhibitor significantly diminished the proliferative and differentiation-promoting effects of LA,confirming the critical role of this pathway.β-catenin knockdown experiments further substantiated its central role in LA-mediated regulation.Conclusion This study confirms that LA promotes osteoblast proliferation,differentiation,mineralization,and migration by activating the Wnt/β-catenin signaling pathway. 展开更多
关键词 Lithospermic acid osteoblasts cell proliferation cell differentiation Wnt/β-catenin signaling pathway
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DLG3 Promotes Breast Cancer Cell Proliferation and Migration by Mediating STAT3 Activation 认领 引用
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作者 Khalid Idris GIDADO Rabiu LAWAN +4 位作者 PENG Xixia ZHANG Ziyang WAN Xiaochun LU Zhen ZHANG Guizhong 《集成技术》 CAS 2026年第1期41-55,共15页
Breast cancer(BRCA)is characterized by high heterogeneity,with aggressive subtypes frequently showing poor prognosis and resistance to conventional therapies,making the discovery of new therapeutic targets and strateg... Breast cancer(BRCA)is characterized by high heterogeneity,with aggressive subtypes frequently showing poor prognosis and resistance to conventional therapies,making the discovery of new therapeutic targets and strategies imperative.Although elevated expression of discs large homolog 3(DLG3)has been reported in BRCA,its functional role in disease progression remains unclear.We performed bioinformatic analyses of clinical datasets to evaluate the prognostic significance of DLG3 expression in BRCA patients.In vitro gain-and loss-of-function experiments were conducted to assess the impact of DLG3 on BRCA cell proliferation,migration,and colony formation.Transcriptomic profiling,coupled with pharmacological inhibition,was employed to identify and validate downstream signaling pathways.Additionally,we extended our validation to an in vivo model to assess the role of DLG3 in tumor progression.We found that elevated DLG3 levels correlated with poor prognosis in breast cancer patients.Functionally,DLG3 overexpression significantly promoted cell proliferation and migration in estrogen receptor-positive MCF7 and triple-negative MDA-MB-231 breast cancer cells,whereas its knockdown suppressed these effects.Transcriptomic analyses revealed that DLG3 activates signal transducer and activator of transcription 3(STAT3)signaling,a finding further corroborated by Western blot.Critically,treatment with the STAT3 inhibitor Stattic attenuated DLG3-driven proliferation and migration,supporting a DLG3-STAT3 oncogenic axis.Furthermore,in vivo studies validated the role of DLG3 in promoting tumor growth and its correlation with elevated STAT3 signaling,consistent with our in vitro findings.Our findings establish DLG3 as a novel driver of breast cancer progression that directly activates STAT3 signaling.DLG3 thus represents both a potential prognostic biomarker and a promising therapeutic target for aggressive breast cancer subtypes,including triple-negative breast cancer. 展开更多
关键词 breast cancer DLG3 STAT3 proliferation migration
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Retraction:miR-26b Mimic Inhibits Glioma Proliferation In Vitro and In Vivo Suppressing COX-2 Expression 认领 引用
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作者 Oncology Research Editorial Office 《Oncology Research》 SCIE 2026年第6期783-783,共1页
The published article titled“miR-26bMimic Inhibits Glioma Proliferation In Vitro and In Vivo Suppressing COX-2 Expression”has been retracted from Oncology Research,Vol.27,No.2,2019,pp.147–155.DOI:10.3727/096504017X... The published article titled“miR-26bMimic Inhibits Glioma Proliferation In Vitro and In Vivo Suppressing COX-2 Expression”has been retracted from Oncology Research,Vol.27,No.2,2019,pp.147–155.DOI:10.3727/096504017X15021536183517 URL:http://gffzz9e48629005df441asfc0nwk5cbpk96vxw.ffgz.tsg.suse.edu.cn/or/v27n2/48639 Following the publication,concerns have been raised about a number of figures in this article.An unexpected area of similarity was identified in terms of the cellular data,where the results from differently performed experiments were intended to have been shown,although the areas immediately surrounding this area featured comparatively different distributions of cells. 展开更多
关键词 cellular datawhere glioma proliferation cox expression retraction figures
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Retraction:MicroRNA-133b Inhibits Proliferation,Cellular Migration,and Invasion via Targeting LASP1 in Hepatocarcinoma Cells 认领 引用
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作者 Oncology Research Editorial Office 《Oncology Research》 SCIE 2026年第1期621-621,共1页
The published article titled“MicroRNA-133b Inhibits Proliferation,Cellular Migration,and Invasion via Targeting LASP1 in Hepatocarcinoma Cells”has been retracted from Oncology Research,Vol.25,No.8,2017,pp.1269–1282.
关键词 lasp cellular migration proliferation invasion hepatocarcinoma cells targeting lasp microrna b
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Retraction:MicroRNA 125a-5p Inhibits Cell Proliferation and Induces Apoptosis in Hepatitis B Virus-Related Hepatocellular Carcinoma by Downregulation of ErbB3 认领 引用
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作者 Oncology Research Editorial Office 《Oncology Research》 SCIE 2026年第4期893-893,共1页
Published:23 March 2026 The published article titled“MicroRNA 125a-5p Inhibits Cell Proliferation and Induces Apoptosis in Hepatitis B Virus-Related Hepatocellular Carcinoma by Downregulation of ErbB3”has been retra... Published:23 March 2026 The published article titled“MicroRNA 125a-5p Inhibits Cell Proliferation and Induces Apoptosis in Hepatitis B Virus-Related Hepatocellular Carcinoma by Downregulation of ErbB3”has been retracted from Oncology Research,Vol.27,No.4,2019,pp.449-458.DOI:10.3727/096504017X15016337254623 URL:http://gffzz9e48629005df441asfc0nwk5cbpk96vxw.ffgz.tsg.suse.edu.cn/or/v27n4/48558. 展开更多
关键词 hepatocellular carcinoma erbb cell proliferation hepatitis b virus downregulation erbb apoptosis induces apoptosis microrna p
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Retraction: miR-325-3p Promotes the Proliferation, Invasion, and EMT of Breast Cancer Cells by Directly Targeting S100A2 认领 引用
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《Oncology Research》 SCIE 2026年第5期860-860,共1页
The published article titled“miR-325-3p Promotes the Proliferation,Invasion,and EMT of Breast Cancer Cells by Directly Targeting S100A2”has been retracted from Oncology Research,Vol.28,No.7-8,2020,pp.731-744.DOI:10.... The published article titled“miR-325-3p Promotes the Proliferation,Invasion,and EMT of Breast Cancer Cells by Directly Targeting S100A2”has been retracted from Oncology Research,Vol.28,No.7-8,2020,pp.731-744.DOI:10.3727/096504020X16100888208039 URL:http://gffzz9e48629005df441asfc0nwk5cbpk96vxw.ffgz.tsg.suse.edu.cn/or/v28n7-8/48464. 展开更多
关键词 breast cancer cells directly targeting s EMT proliferation invasion miR p S
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Retraction: miR-206 Inhibits Cell Proliferation, Migration, and Invasion by Targeting BAG3 in Human Cervical Cancer 认领 引用
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《Oncology Research》 SCIE 2026年第8期638-638,共1页
Oncology Research Editorial Office Published:16 July 2026 The published article titled“miR-206 Inhibits Cell Proliferation,Migration,and Invasion by Targeting BAG3 in Human Cervical Cancer”has been retracted from On... Oncology Research Editorial Office Published:16 July 2026 The published article titled“miR-206 Inhibits Cell Proliferation,Migration,and Invasion by Targeting BAG3 in Human Cervical Cancer”has been retracted from Oncology Research,Vol.26,No.6,2018,pp.923-931.DOI:10.3727/096504017X15143731031009 URL:http://gffzz9e48629005df441asfc0nwk5cbpk96vxw.ffgz.tsg.suse.edu.cn/or/v26n6/56705 Following the publication,concerns have been raised about a number of figures in this article.An unexpected area of similarity was identified in terms of the cellular data,where the results from differently performed experiments were intended to have been shown,although the areas immediately surrounding this area featured comparatively different distributions of cells.In addition,the western blots in this article were presented with atypical,unusually shaped and possibly anomalous protein bands in many cases.The authors were contacted and invited to comment on the concerns raised and to provide the original,unmodified figures,but did not respond.The Editors-in-Chief therefore no longer have confidence in the integrity of the data in this article and decided to retract this article. 展开更多
关键词 cervical cancer figure similarity cell invasion cellular data cell migration targeting bag cell proliferation bag
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Retraction:Long Noncoding RNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation and Invasion in Gastric Cancer via Negatively Modulating miRNA-145-5p 认领 引用
19
作者 Oncology Research Editorial Office 《Oncology Research》 SCIE 2026年第7期741-741,共1页
The published article titled“Long Noncoding RNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation and Invasion in Gastric Cancer via Negatively Modulating miRNA-145-5p”has been retracted from Oncology Research,... The published article titled“Long Noncoding RNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation and Invasion in Gastric Cancer via Negatively Modulating miRNA-145-5p”has been retracted from Oncology Research,Vol.25,No.5,2017,pp.789–798. 展开更多
关键词 taurine upregulated gene cell invasion gastric cancer long noncoding rna cell proliferation microRNA p
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Retraction:Knockdown of Cyclin-Dependent Kinase Inhibitor 3 Inhibits Proliferation and Invasion in Human Gastric Cancer Cells 认领 引用
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作者 Oncology Research Editorial Office 《Oncology Research》 SCIE 2026年第7期740-740,共1页
The published article titled“Knockdown of Cyclin-Dependent Kinase Inhibitor 3 Inhibits Proliferation and Invasion in Human Gastric Cancer Cells”has been retracted from Oncology Research,Vol.25,No.5,2017,pp.721–731.
关键词 cyclin dependent kinase inhibitor human gastric cancer cells invasion proliferation
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