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A DNA Damage-responsive Long Non-coding RNA lnc-DUSP6 Promotes Cisplatin-induced DNA Damage Repair and Chemoresistance 认领 引用
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作者 XU Shun WU Wei-Jia +8 位作者 YANG Hai-Qing HUANG Hai-Jiao YE Li-Wen ZHU Yue SHEN Jia-En ZHENG Xiao-Li HUANG Xiao-Lu SHEN Han-Lian LI Yu-Ting 《中国生物化学与分子生物学报》 CAS CSCD 北大核心 2026年第2期295-307,共13页
Genomic destabilization and defective DNA repair are the most prominent features of tumour cells and are exploited by various chemotherapy drugs for cancer therapy.Long non-coding RNA(lncR-NAs)have emerged as powerful... Genomic destabilization and defective DNA repair are the most prominent features of tumour cells and are exploited by various chemotherapy drugs for cancer therapy.Long non-coding RNA(lncR-NAs)have emerged as powerful regulators of gene expression and are thus involved in diverse biological processes.Recent studies have demonstrated that several lncRNAs play critical roles in DNA repair.Nonetheless,the relationship between DNA damage-responsive lncRNAs and chemoresistance remains poorly defined.In this study,we established four different DNA damage models triggered by cisplatin(DDP),H2O2,neocarzinostatin(NCS)or ultraviolet(UV)irradiation and identified a specific upregu-lated lncRNA(lnc-DUSP6)involved in the cisplatin-induced DNA damage response.Furthermore,loss-or gain-of-function experiments confirmed that lnc-DUSP6 enhanced DNA repair and cell survival under cisplatin treatment,thus promoting cisplatin resistance.Mechanistically,an RNA immunoprecipitation(RIP)assay revealed that lnc-DUSP6 directly interacts with DUSP6(Dual Specificity Phosphatase 6),which is closely associated with cisplatin sensitivity.Additionally,overexpression of DUSP6 significantly rescued the effects of lnc-DUSP6 silencing on DNA repair and cell survival under cisplatin treatment.O-verall,our results show the effect and underlying mechanism of lnc-DUSP6 in cisplatin resistance:lnc-DUSP6 promotes cisplatin-induced DNA damage repair and cisplatin resistance by stabilizing DUSP6,which is highly clinically important for enhancing the efficacy of cisplatin for cancers. 展开更多
关键词 long non-coding RNA(lncRNAs) chemoresistance dual specificity protein phosphatase 6(DUSP6) lnc-DUSP6 DNA damage response(DDR)
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Long noncoding RNA X-inactive specific transcript regulates NLR family pyrin domain containing 3/caspase-1-mediated pyroptosis in diabetic nephropathy 认领 引用 被引量：11
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作者 Jia Xu Qin Wang +4 位作者 Yi-Fan Song Xiao-Hui Xu He Zhu Pei-Dan Chen Ye-Ping Ren 《World Journal of Diabetes》 SCIE 2022年第4期358-375,共18页
BACKGROUND NLRP3-mediated pyroptosis is recognized as an essential modulator of renal disease pathology.Long noncoding RNAs(lncRNAs)are active participators of diabetic nephropathy(DN).X inactive specific transcript(X... BACKGROUND NLRP3-mediated pyroptosis is recognized as an essential modulator of renal disease pathology.Long noncoding RNAs(lncRNAs)are active participators of diabetic nephropathy(DN).X inactive specific transcript(XIST)expression has been reported to be elevated in the serum of DN patients.AIM To evaluate the mechanism of lncRNA XIST in renal tubular epithelial cell(RTEC)pyroptosis in DN.METHODS A DN rat model was established through streptozotocin injection,and XIST was knocked down by tail vein injection of the lentivirus LV sh-XIST.Renal metabolic and biochemical indices were detected,and pathological changes in the renal tissue were assessed.The expression of indicators related to inflammation and pyroptosis was also detected.High glucose(HG)was used to treat HK2 cells,and cell viability and lactate dehydrogenase(LDH)activity were detected after silencing XIST.The subcellular localization and downstream mechanism of XIST were investigated.Finally,a rescue experiment was carried out to verify that XIST regulates NLR family pyrin domain containing 3(NLRP3)/caspase-1-mediated RTEC pyroptosis through the microRNA-15-5p(miR-15b-5p)/Toll-like receptor 4(TLR4)axis.RESULTS XIST was highly expressed in the DN models.XIST silencing improved renal metabolism and biochemical indices and mitigated renal injury.The expression of inflammation and pyroptosis indicators was significantly increased in DN rats and HG-treated HK2 cells;cell viability was decreased and LDH activity was increased after HGtreatment. Silencing XIST inhibited RTEC pyroptosis by inhibiting NLRP3/caspase-1. Mechanistically,XIST sponged miR-15b-5p to regulate TLR4. Silencing XIST inhibited TLR4 by promotingmiR-15b-5p. miR-15b-5p inhibition or TLR4 overexpression averted the inhibitory effect ofsilencing XIST on HG-induced RTEC pyroptosis.CONCLUSIONSilencing XIST inhibits TLR4 by upregulating miR-15b-5p and ultimately inhibits renal injury inDN by inhibiting NLRP3/caspase-1-mediated RTEC pyroptosis. 展开更多
关键词 Diabetic nephropathy Pyroptosis Renal tubular epithelial cell Long noncoding RNA X-inactive specific transcript microRNA-15b-5p Toll-like receptor 4 NLR family pyrin domain containing 3/caspase-1 pathway
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Long non-coding RNA GAS5 promotes neuronal apoptosis in spinal cord injury via the miR-21/PTEN axis 认领 引用
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作者 Ying-Jie Wang Zhong-Zheng Zhi +2 位作者 Tao Liu Jian Kang Guang-Hui Xu 《World Journal of Orthopedics》 2025年第5期80-92,共13页
BACKGROUND Spinal cord injury(SCI)is a severe and permanent trauma that often leads to significant motor,sensory,and autonomic dysfunction.Neuronal apoptosis is a major pathomechanism underlying secondary injury in SC... BACKGROUND Spinal cord injury(SCI)is a severe and permanent trauma that often leads to significant motor,sensory,and autonomic dysfunction.Neuronal apoptosis is a major pathomechanism underlying secondary injury in SCI.Long non-coding RNAs(lncRNAs)have emerged as key regulators of gene expression and cellular processes,including apoptosis.However,the role of lncRNA growth arrest-specific transcript 5(GAS5)in SCI-induced neuronal apoptosis remains unclear.AIM To investigate the role of lncRNA GAS5 in SCI-induced neuronal apoptosis via its interaction with microRNA(miR)-21 and the phosphatase and tensin homolog(PTEN)/AKT pathway.METHODS SCI rat models and hypoxic neuronal cell models were established.Motor function was assessed using the Basso-Beattie-Bresnahan score.Expression levels of GAS5,miR-21,PTEN,caspase 3,B-cell lymphoma 2(Bcl-2),Bcl-2-associated X protein(Bax),and AKT were measured using quantitative PCR or Western blot analysis.Neuronal apoptosis was determined by TUNEL staining.Dual-luciferase reporter assays validated GAS5-miR-21 binding.Knockdown and overexpression experiments explored the functional effects of the GAS5/miR-21 axis.RESULTS GAS5 was significantly upregulated in the spinal cord following SCI,coinciding with increased neuronal apoptosis and decreased AKT activation.In vitro experiments demonstrated that GAS5 acted as a molecular sponge for miR-21,leading to increased PTEN expression and inhibition of the AKT signaling pathway,thereby promoting apoptosis.In vivo,GAS5 knockdown attenuated neuronal apoptosis,enhanced AKT activation,and improved motor function recovery in SCI rats.CONCLUSION GAS5 promotes neuronal apoptosis in SCI by binding to miR-21 and upregulating PTEN expression,inhibiting the AKT pathway.Targeting GAS5 may represent a novel therapeutic strategy for SCI. 展开更多
关键词 Spinal cord injury Long non-coding RNA Growth arrest-specific transcript 5 MicroRNA-21 Neuronal apoptosis
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Effects of long non-coding RNA myocardial infarction-associated transcript on retinal neovascularization in a newborn mouse model of oxygen-induced retinopathy 认领 引用 被引量：10
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作者 Yu Di Yue Wang +1 位作者 Xue Wang Qing-Zhu Nie 《Neural Regeneration Research》 SCIE CAS CSCD 2021年第9期1877-1881,共5页
Whether long non-coding RNA myocardial infarction-associated transcript is involved in oxygen-induced retinopathy remains poorly understood. To validate this hypothesis, we established a newborn mouse model of oxygen-... Whether long non-coding RNA myocardial infarction-associated transcript is involved in oxygen-induced retinopathy remains poorly understood. To validate this hypothesis, we established a newborn mouse model of oxygen-induced retinopathy by feeding in an oxygen concentration of 75 ± 2% from postnatal day 8 to postnatal day 12, followed by in normal air. On postnatal day 11, the mice were injected with the myocardial infarction-associated transcript siRNA plasmid via the vitreous cavity to knockdown long non-coding RNA myocardial infarction-associated transcript. Myocardial infarction-associated transcript siRNA transcription significantly inhibited myocardial infarctionassociated transcript mRNA expression, reduced the phosphatidylinosital-3-kinase, phosphorylated Akt and vascular endothelial growth factor immunopositivities, protein and mRNA expression, and alleviated the pathological damage to the retina of oxygen-induced retinopathy mouse models. These findings suggest that myocardial infarction-associated transcript is likely involved in the retinal neovascularization in retinopathy of prematurity and that inhibition of myocardial infarction-associated transcript can downregulate phosphatidylinosital-3-kinase, phosphorylated Akt and vascular endothelial growth factor expression levels and inhibit neovascularization. This study was approved by the Animal Ethics Committee of Shengjing Hospital of China Medical University, China(approval No. 2016 PS074 K) on February 25, 2016. 展开更多
关键词 long non-coding RNA myocardial infarction-associated transcript neovascularization neurovascular prematurity retinopathy vascular development vascular endothelial growth factor
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Molecular insights into hyperglycemia-associated coronary heart disease:From glycemic variability and heart rate dynamics to long noncoding RNAs 认领 引用
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作者 Shilpy Singh Varun Kumar Sharma Dharmsheel Shrivastav 《World Journal of Diabetes》 SCIE 2026年第3期1-5,共5页
The retrospective study was done by Li and Zhang suggested a complex association between by measuring heart rate dynamics and blood glucose variability in coronary heart disease with type 2 diabetes patients.The resul... The retrospective study was done by Li and Zhang suggested a complex association between by measuring heart rate dynamics and blood glucose variability in coronary heart disease with type 2 diabetes patients.The results suggest that disturbance in measurement of glucose like mean amplitude of glycemic excursions,mean of daily differences,largest amplitude of glycemic excursions and mean postprandial glucose excursions are relatively associated with dysregulated heart rate or heart rate variability and impaired cardiac function and can be an important biomarker for complication of cardiovascular diseases and immediate death.Further expanding these associations,recent molecular biological studies suggested that long non-coding RNAs PSMB8-AS-1,transcription factors PSMB9/ZEB-1/NONO linked with inflammation and vascular instability,and increase the risk of cardiovascular diseases.This study aims to explore the role of PSMB8-AS-1 and transcription factors PSMB9/ZEB-1/NONO in hyperglycemiaassociated coronary heart disease. 展开更多
关键词 Long non-coding RNA Transcription factor Diabetes mellitus Coronary artery disease Glycemic variability
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Danhongqing formula alleviates cholestatic liver fibrosis by downregulating long non-coding RNA H19 derived from cholangiocytes and inhibiting hepatic stellate cell activation 认领 引用 被引量：3
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作者 Meng Li Yang Zhou +2 位作者 Hui Zhu Lie-ming Xu Jian Ping 《Journal of Integrative Medicine》 SCIE CAS CSCD 2024年第2期188-198,共11页
Objective:This study explores the mechanism of action of Danhongqing formula(DHQ),a compoundbased Chinese medicine formula,in the treatment of cholestatic liver fibrosis.Methods:In vivo experiments were conducted usin... Objective:This study explores the mechanism of action of Danhongqing formula(DHQ),a compoundbased Chinese medicine formula,in the treatment of cholestatic liver fibrosis.Methods:In vivo experiments were conducted using 8-week-old multidrug resistance protein 2 knockout(Mdr2-/-)mice as an animal model of cholestatic liver fibrosis.DHQ was administered orally for 8 weeks,and its impact on cholestatic liver fibrosis was evaluated by assessing liver function,liver histopathology,and the expression of liver fibrosis-related proteins.Real-time polymerase chain reaction,Western blot,immunohistochemistry and other methods were used to observe the effects of DHQ on long non-coding RNA H19(H19)and signal transducer and activator of transcription 3(STAT3)phosphorylation in the liver tissue of Mdr2-/-mice.In addition,cholangiocytes and hepatic stellate cells(HSCs)were cultured in vitro to measure the effects of bile acids on cholangiocyte injury and H19 expression.Cholangiocytes overexpressing H19 were constructed,and a conditioned medium containing H19 was collected to measure its effects on STAT3 protein expression and cell activation.The intervention effect of DHQ on these processes was also investigated.HSCs overexpressing H19 were constructed to measure the impact of H19 on cell activation and assess the intervention effect of DHQ.Results:DHQ alleviated liver injury,ductular reaction,and fibrosis in Mdr2-/-mice,and inhibited H19expression,STAT3 expression and STAT3 phosphorylation.This formula also reduced hydrophobic bile acid-induced cholangiocyte injury and the upregulation of H19,inhibited the activation of HSCs induced by cholangiocyte-derived conditioned medium,and decreased the expression of activation markers in HSCs.The overexpression of H19 in a human HSC line confirmed that H19 promoted STAT3 phosphorylation and HSC activation,and DHQ was able to successfully inhibit these effects.Conclusion:DHQ effectively alleviated spontaneous cholestatic liver fibrosis in Mdr2-/-mice by inhibiting H19 upregulation in cholangiocytes and preventing the inhibition of STAT3 phosphorylation in HSC,thereby suppressing cell activation. 展开更多
关键词 Liver cirrhosis biliary Long non-coding RNA H19 Danhongqing formula Cholangiocyte Hepatic stellate cells STAT3 transcription factor
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Long non-coding RNAs with essential roles in neurodegenerative disorders 认领 引用 被引量：1
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作者 Wandi Xiong Lin Lu Jiali Li 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第6期1212-1220,共9页
Recently,with the advent of high-resolution and high-throughput sequencing technologies,an increasing number of long non-coding RNAs(lncRNAs)have been found to be involved in the regulation of neuronal function in the... Recently,with the advent of high-resolution and high-throughput sequencing technologies,an increasing number of long non-coding RNAs(lncRNAs)have been found to be involved in the regulation of neuronal function in the central nervous system with specific spatiotemporal patterns,across different neurodegenerative diseases.However,the underlying mechanisms of lncRNAs during neurodegeneration remain poorly understood.This review provides an overview of the current knowledge of the biology of lncRNAs and focuses on introducing the latest identified roles,regulatory mechanisms,and research status of lncRNAs in Alzheimer's disease,Parkinson's disease,Huntington's disease,and amyotrophic lateral sclerosis.Finally,this review discusses the potential values of lncRNAs as diagnostic biomarkers and therapeutic targets for neurodegenerative diseases,hoping to provide broader implications for developing effective treatments. 展开更多
关键词 Alzheimer's disease amyotrophic lateral sclerosis biomarker Huntington's disease long non-coding RNAs neurodegenerative diseases Parkinson's disease therapy transcriptional regulation translational regulation
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Unexpected Roles of Long Non-Coding RNAs in Cancer Biology 认领 引用 被引量：1
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作者 戚颖 康亚妮 赵小东 《Journal of Shanghai Jiaotong university(Science)》 EI 2014年第5期544-549,共6页
Recent studies show that long non-coding RNAs(lncRNAs) play important roles in the regulation of various biological processes, including chromatin remodeling, dosage-compensation, imprinting, and epigenetic regulation... Recent studies show that long non-coding RNAs(lncRNAs) play important roles in the regulation of various biological processes, including chromatin remodeling, dosage-compensation, imprinting, and epigenetic regulation. Aberrant expression of lncRNAs is involved in many complex human diseases, including cancer. In this review, we summarized recent progress on lncRNAs detection methodology with emphasis on their functions and potential implication in cancer diagnosis and therapy. 展开更多
关键词 long non-coding RNA （lncRNAs） epigenetics transcription carcinomas
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Regulatory mechanisms of long non-coding RNAs 认领 引用
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作者 Zhigang Luo 《Oncology and Translational Medicine》 CAS 2019年第3期147-151,共5页
Long non-coding RNAs(lncRNAs) belong to a large and complex family of RNAs, which play many important roles in regulating gene expression. However, the mechanism underlying the dynamic expression of lncRNAs is still n... Long non-coding RNAs(lncRNAs) belong to a large and complex family of RNAs, which play many important roles in regulating gene expression. However, the mechanism underlying the dynamic expression of lncRNAs is still not very clear. In order to identify lncRNAs and clarify the mechanisms involved, we collected basic information and highlighted the mechanisms underlying lncRNA expression and regulation. Overall, lncRNAs are regulated by several similar transcription factors and protein-coding genes. Epigenetic modification(DNA methylation and histone modification) can also downregulate lncRNA levels in tissues and cells. Moreover, lncRNAs may be degraded or cleaved via interaction with miRNAs and miRNAassociated protein complexes. Furthermore, alternative RNA splicing(AS) may play a significant role in the post-transcriptional regulation of lncRNAs. 展开更多
关键词 long non-coding RNAs(lncRNAs) regulatory mechanisms transcriptional factors chromatin state,alternative splicing RNA editing,microRNA(miRNA)
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Role of long non-coding RNAs in non-alcoholic fatty liver disease 认领 引用
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作者 Anju Mullath Murali Krishna 《World Journal of Meta-Analysis》 2024年第3期1-5,共5页
Non-alcoholic fatty liver disease(NAFLD)is emerging as a common cause of chronic liver disease in children and adults.NAFLD can progress to steatohepa-titis and potentially even hepatocellular carcinoma.Early identifi... Non-alcoholic fatty liver disease(NAFLD)is emerging as a common cause of chronic liver disease in children and adults.NAFLD can progress to steatohepa-titis and potentially even hepatocellular carcinoma.Early identification of pati-ents at risk for progressive disease is crucial for managing NAFLD.Recent studies have identified long noncoding RNAs(lncRNAs),circular RNAs,and microRNAs as playing important roles in the pathogenesis of NAFLD.These noncoding RNAs are involved in modulating several metabolic pathways such as hepatic glucose and lipid metabolism,oxidative stress,and even carcinogenesis.Elevated levels of lncARSR and lncRNA nuclear-enriched abundant transcript 1 have been found in patients with NAFLD.In addition,lncRNAs such as PRYP4-3 and RP11-128N14.5 can distinguish patients with NAFLD from healthy indi-viduals.Increased MEG3 expression has been observed in both NAFLD and non-alcoholic steatohepatitis,suggesting that it may help predict patients at risk for disease progression.With advances in transcriptomics,we may discover additional targets to help in the identification and prognostication of NAFLD. 展开更多
关键词 Long noncoding RNA Non-alcoholic fatty liver disease Plasmacytoma variant translocation 1 Nuclear-enriched abundant transcript 1 Muscle-and adiposeassociated long intergenic non-coding RNA H19
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lncRNA XIST靶向miR-21-5p对脂多糖诱导的心肌细胞凋亡、炎症反应的影响 认领 引用
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作者 周晓铎 张松雨 +2 位作者 李燕 王琰淏 韩克丽 《中国免疫学杂志》 CAS CSCD 北大核心 2026年第4期782-787,共6页
目的:探究长链非编码RNA(lncRNA)X染色体失活特异转录本(XIST)对脂多糖(LPS)诱导的心肌细胞凋亡、炎症反应的影响及潜在机制。方法:体外培养大鼠心肌H9c2细胞,分为对照组、LPS组、si-NC组、si-XIST组、si-XIST+anti-NC组、si-XIST+anti-... 目的:探究长链非编码RNA(lncRNA)X染色体失活特异转录本(XIST)对脂多糖(LPS)诱导的心肌细胞凋亡、炎症反应的影响及潜在机制。方法:体外培养大鼠心肌H9c2细胞,分为对照组、LPS组、si-NC组、si-XIST组、si-XIST+anti-NC组、si-XIST+anti-miR-21-5p组。CCK-8法测定细胞活力;流式细胞术测定细胞凋亡;ELISA检测上清炎症因子IL-1β、IL-6和TNF-α水平;RT-qPCR检测细胞lncRNA XIST、miR-21-5p、程序性细胞死亡蛋白4(PDCD4)mRNA表达;Western blot检测细胞PDCD4、BCL2相关X蛋白(Bax)、B细胞淋巴瘤-2(Bcl-2)、cleaved caspase-3、cleaved caspase-9蛋白表达。结果:与对照组相比,LPS组H9c2细胞活力、Bcl-2蛋白水平降低,凋亡率、上清IL-1β、TNF-α和IL-6水平、lncRNA XIST、PDCD4 mRNA和蛋白表达、Bax、cleaved caspase-3和cleaved caspase-9蛋白水平升高(P<0.05);与si-NC组相比,si-XIST组H9c2细胞活力、Bcl-2蛋白水平升高,凋亡率、上清IL-1β、TNF-α和IL-6水平、lncRNA XIST、PDCD4 mRNA和蛋白表达、Bax、cleaved caspase-3和cleaved caspase-9蛋白水平降低(P<0.05);下调miR-21-5p可明显减弱lncRNA XIST敲低对LPS诱导的H9c2细胞凋亡和炎症反应的抑制作用。结论:敲低lncRNA XIST可能通过上调miR-21-5p,抑制PDCD4表达,减轻LPS诱导的H9c2细胞炎症反应,并抑制细胞凋亡。 展开更多
关键词 长链非编码RNA X染色体失活特异转录本 脂多糖 心肌细胞 miR-21-5p 凋亡 炎症反应
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lncRNA XIST靶向miR-182-5p/HIF-2α分子轴对滋养层细胞生物学行为特性影响的机制研究 认领 引用
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作者 黄燕 张林静 +2 位作者 汪洪林 张婷 李波 《中国比较医学杂志》 CAS 北大核心 2026年第6期11-20,共10页
目的探究长链非编码RNA(lncRNA)X染色体失活特异性转录本(XIST)调控滋养层细胞生物学活性的分子机制。方法体外培养人绒毛膜滋养层细胞HTR-8/Svneo,分为对照组、干扰空载组(转染siNC)和si-XIST-1组(转染si-XIST-1)、si-XIST-1+anti-NC组... 目的探究长链非编码RNA(lncRNA)X染色体失活特异性转录本(XIST)调控滋养层细胞生物学活性的分子机制。方法体外培养人绒毛膜滋养层细胞HTR-8/Svneo,分为对照组、干扰空载组(转染siNC)和si-XIST-1组(转染si-XIST-1)、si-XIST-1+anti-NC组(共转染si-XIST-1和anti-NC)、si-XIST-1+anti-182-5p组(共转染si-XIST-1和anti-182-5p)。采用RT-qPCR检测细胞中XIST、miR-182-5p和低氧诱导因子2α(HIF-2α)mRNA表达;CCK-8实验和EdU实验检测细胞增殖活力;流式细胞术检测细胞凋亡;划痕愈合实验、Transwell实验检测细胞迁移、侵袭能力;Western blot检测细胞中HIF-2α、cleaved-caspase-3、Bcl-2、Bax、基质金属蛋白(MMP)-2、MMP-9蛋白表达;双荧光素酶报告实验验证miR-182-5p与XIST、HIF-2α的靶向关系。结果与对照组、干扰空载组比较,si-XIST-1组XIST、HIF-2αmRNA水平、凋亡率及HIF-2α、cleaved-caspase-3、Bax蛋白水平降低,miR-182-5p水平、细胞活力、EdU阳性率、划痕愈合率、侵袭细胞数及Bcl-2、MMP-2、MMP-9蛋白水平升高(P<0.05);与si-XIST-1组和si-XIST-1+anti-NC组比较,si-XIST-1+anti-182-5p组HIF-2αmRNA水平、凋亡率及HIF-2α、cleaved-caspase-3、Bax蛋白水平升高,miR-182-5p水平、细胞活力、EdU阳性率、划痕愈合率、侵袭细胞数及Bcl-2、MMP-2、MMP-9蛋白水平降低(P<0.05)。lncRNA XIST可靶向HTR-8/Svneo细胞中的miR-182-5p,HIF-2α是miR-182-5p的靶标。结论敲低lncRNA XIST可能是通过竞争性结合miR-182-5p来抑制HIF-2α表达,进而增强HTR-8/Svneo细胞增殖、迁移和侵袭能力,并抑制细胞凋亡。 展开更多
关键词 子痫前期 长链非编码RNA X染色体失活特异性转录本 microRNA-182 低氧诱导因子2α 滋养层细胞
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lncRNA GAS6-AS1调节miR-326/E2F1轴对神经母细胞瘤细胞增殖、迁移和侵袭影响的实验研究 认领 引用
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作者 安艳晓 祁艳卫 仲智勇 《现代检验医学杂志》 CAS 2026年第1期46-50,69,共5页
目的探究长链非编码RNA(lncRNA)生长阻滞特异性基因6反义RNA1(GAS6-AS1)通过调节微小RNA-326(miR-326)/E2F转录因子1(E2F1)轴对神经母细胞瘤(NB)细胞增殖、迁移和侵袭的影响。方法收集23例2021年8月~2023年1月在河北省儿童医院接受治疗... 目的探究长链非编码RNA(lncRNA)生长阻滞特异性基因6反义RNA1(GAS6-AS1)通过调节微小RNA-326(miR-326)/E2F转录因子1(E2F1)轴对神经母细胞瘤(NB)细胞增殖、迁移和侵袭的影响。方法收集23例2021年8月~2023年1月在河北省儿童医院接受治疗的NB患儿瘤组织及瘤旁组织,实时荧光定量聚合酶链反应(qRT-PCR)检测NB组织和细胞中lncRNA GAS6-AS1、miR-326、E2F1 mRNA表达水平并用双荧光素酶实验检测三者间的关系。将SK-N-SH细胞随机分为对照(control)组、短发夹RNA阴性对照(sh-NC)组、GAS6-AS1短发夹RNA(sh-GAS6-AS1)组、sh-GAS6-AS1+抑制剂阴性对照(anti-NC)组、sh-GAS6-AS1+miR-326抑制剂(anti-miR-326)组。qRT-PCR检测各组细胞中lncRNA GAS6-AS1和miR-326表达水平,克隆形成实验、划痕实验、Transwell实验及蛋白免疫印迹法分别检测NB细胞增殖、迁移、侵袭及E2F1、细胞周期蛋白D1(Cyclin D1)、基质金属蛋白酶(MMP)-2、MMP-9蛋白表达;构建裸鼠移植瘤模型,随机将小鼠分为sh-NC组和sh-GAS6-AS1组,qRT-PCR检测移植瘤组织中lncRNA GAS6-AS1和miR-326水平,免疫组化检测移植瘤组织中E2F1蛋白表达。结果与瘤旁组织和人正常神经细胞视网膜色素上皮细胞D-407比较,NB瘤组织和SK-N-SH细胞中lncRNA GAS6-AS1水平、E2F1 mRNA表达升高,miR-326表达降低,差异具有统计学意义(t=7.221~53.271,均P<0.05);lncRNA GAS6-AS1及E2F1与miR-326存在靶向关系。与sh-NC组比较,sh-GAS6-AS1组细胞克隆形成数目、划痕愈合率、侵袭细胞数目、lncRNA GAS6-AS1、E2F1、Cyclin D1、MMP-2、MMP-9表达下降,miR-326表达上升,差异具有统计学意义(q=8.706~16.489,均P<0.05)。与sh-GAS6-AS1+anti-NC组比较,sh-GAS6-AS1+anti-miR-326组克隆形成数目、划痕愈合率、侵袭细胞数目、E2F1、Cyclin D1、MMP-2、MMP-9表达升高,miR-326表达降低,差异具有统计学意义(q=4.173~13.407,均P<0.05)。裸鼠实验显示,与sh-NC组比较,sh-GAS6-AS1组肿瘤质量、体积均下降,lncRNA GAS6-AS1、E2F1表达下调,miR-326表达上调,差异具有统计学意义(t=8.684~13.494,均P<0.05)。结论抑制lncRNA GAS6-AS1表达可能通过靶向miR-326/E2F1轴抑制NB细胞增殖、迁移、侵袭。 展开更多
关键词 神经母细胞瘤 长链非编码RNA生长阻滞特异性基因6反义RNA1 微小RNA-326 E2F转录因子1 增殖 迁移 侵袭
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lncRNA GAS5对人心脏微血管内皮细胞缺血再灌注损伤的影响及机制实验研究 认领 引用
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作者 范芮 马玉龙 +1 位作者 赖红梅 向阳 《陕西医学杂志》 CAS 2026年第5期605-610,共6页
目的:探讨长链非编码RNA(lncRNA)生长阻滞特异性转录因子5(GAS5)对人心脏微血管内皮细胞(HCMEC)缺血再灌注(IR)损伤的影响及其可能的机制。方法:选取HCMEC,分为正常对照组(常规培养,无干预)、模型组(建立细胞IR损伤模型)、阴性对照组(IR... 目的:探讨长链非编码RNA(lncRNA)生长阻滞特异性转录因子5(GAS5)对人心脏微血管内皮细胞(HCMEC)缺血再灌注(IR)损伤的影响及其可能的机制。方法:选取HCMEC,分为正常对照组(常规培养,无干预)、模型组(建立细胞IR损伤模型)、阴性对照组(IR+转染阴性对照慢病毒)、GAS5过表达组(IR+转染lncRNA GAS5过表达慢病毒)、GAS5干扰组(IR+转染lncRNA GAS5干扰慢病毒)。观察各组细胞形态学特征;RT-qPCR检测各组细胞GAS5 mRNA水平;ELISA法检测各组细胞炎症因子水平;MTT法检测各组细胞增殖能力;TUNEL法检测各组细胞凋亡能力;Western blot检测各组细胞微管相关蛋白1轻链3(LC3)、Beclin1蛋白表达。结果:正常对照组HCMEC贴壁紧密、形态规则、胞质均匀,无细胞脱落现象;模型组细胞贴壁能力显著下降、细胞皱缩变圆、胞质颗粒增多,且可见部分细胞从培养皿壁脱落;阴性对照组细胞形态与模型组无明显差异;GAS5过表达组上述细胞损伤相关形态学改变明显改善;GAS5干扰组细胞损伤形态较阴性对照组进一步加重。与正常对照组比较,模型组细胞凋亡率、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平升高,细胞增殖率、GAS5 mRNA及LC3、Beclin1蛋白表达水平降低(均P0.05)。GAS5过表达组上述指标变化较阴性对照组改善,而GAS5干扰组较阴性对照组加重(均P<0.05)。结论:上调lncRNA GAS5表达可减轻IR造成的HCMEC损伤,其机制可能与激活细胞自噬有关。 展开更多
关键词 长链非编码RNA生长阻滞特异性转录因子5 缺血再灌注 人心脏微血管内皮细胞 细胞增殖 细胞凋亡 自噬
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多发性子宫肌瘤剔除术前后彩色多普勒超声参数、lncRNA XIST变化对术后复发评估价值 认领 引用
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作者 陈果 王荔 +1 位作者 胡科丹 张柯 《中国妇幼健康研究》 CAS 2026年第3期100-106,共7页
目的分析多发性子宫肌瘤剔除术前后彩色多普勒超声(CDFI)参数、长链非编码RNA X染色体失活特异转录本(lncRNA XIST)变化对术后复发的评估价值。方法选取2022年1月至2024年2月泸州市人民医院收治的196例拟行多发性子宫肌瘤剔除术患者作... 目的分析多发性子宫肌瘤剔除术前后彩色多普勒超声(CDFI)参数、长链非编码RNA X染色体失活特异转录本(lncRNA XIST)变化对术后复发的评估价值。方法选取2022年1月至2024年2月泸州市人民医院收治的196例拟行多发性子宫肌瘤剔除术患者作为研究对象,根据术后6个月是否复发分为复发组和未复发组,采用倾向性评分匹配(PSM)来降低组间选择偏倚。采用Voluson E10型彩色多普勒超声诊断仪测定术前、术后1个月舒张期血流速度(EDV)、收缩期血流速度(PSV)、子宫阻力指数(UtA-RI)、子宫搏动指数(UtA-PI),采用实时荧光定量聚合酶链式反应(qRT-PCR)测定术前、术后1个月lncRNA XIST,采用Logistic回归方程分析CDFI参数、lncRNA XIST与多发性子宫肌瘤剔除术后复发的关系,采用受试者工作特征(ROC)曲线分析模型预测价值。结果术后6个月,研究对象中共有5例失访,55例(28.79%)复发;匹配后复发组术前lncRNA XIST、EDV、PSV、UtA-PI高于未复发组,UtA-RI低于未复发组,差异有统计学意义(t值介于11.733~16.918之间,P<0.05);ROC曲线显示,术前lncRNA XIST、EDV、PSV、UtA-PI、UtA-RI预测多发性子宫肌瘤剔除术后复发的曲线下面积(AUC)分别为0.754、0.766、0.792、0.776、0.742,联合预测的AUC为0.918,灵敏度为81.82%,特异度为92.73%,联合预测AUC高于单独预测(Z值介于2.215~3.340之间,P<0.001);按截断值分组,lncRNA XIST、EDV、PSV、UtA-RI、UtA-PI高值患者复发风险是低值患者的1.647、1.875、1.406、0.700、1.664倍。结论lncRNA XIST、EDV、PSV、UtA-PI、UtA-RI异常均会增加多发性子宫肌瘤剔除术后复发风险,五者联合有助于提高预测价值,指导临床诊治。 展开更多
关键词 子宫肌瘤 多发性 腹腔镜子宫肌瘤剔除术 复发 彩色多普勒超声 长链非编码RNA X染色体失活特异转录本
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lncRNA XIST调控miR-17-5p/FOSL1轴对胆囊癌细胞增殖、迁移和侵袭的影响 认领 引用
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作者 陈李康 姚磊 彭莹莹 《肝胆胰外科杂志》 CAS 2026年第2期115-123,共9页
目的探讨长链非编码RNA(lncRNA)X染色体失活特异性转录本(XIST)调控微小RNA-17-5p(miR-17-5p)/FOS样抗原1(FOSL1)轴对胆囊癌(GBC)细胞增殖、迁移和侵袭的影响。方法qRT-PCR法检测GBC组织和细胞株中mRNA表达;双荧光素酶报告基因实验验证l... 目的探讨长链非编码RNA(lncRNA)X染色体失活特异性转录本(XIST)调控微小RNA-17-5p(miR-17-5p)/FOS样抗原1(FOSL1)轴对胆囊癌(GBC)细胞增殖、迁移和侵袭的影响。方法qRT-PCR法检测GBC组织和细胞株中mRNA表达;双荧光素酶报告基因实验验证lncRNA XIST与miR-17-5p,miR-17-5p与FOSL1的互作;将EH-GB1细胞分为Ctrl组、sh-NC组、sh-XIST组、sh-XIST+inhibitor-NC组、sh-XIST+inhibitor-miR-17-5p组、mimic-NC组、mimic-miR-17-5p组、mimic-miR-17-5p+OE-NC组、mimic-miR-17-5p+OE-FOSL1组。台盼蓝染色和平板克隆实验检测EH-GB1细胞增殖;划痕试验检测EH-GB1细胞迁移;Transwell实验检测EH-GB1细胞侵袭;Western blotting检测EH-GB1细胞中Ki67、Cyclin D1、MMP-2、CD44、FOSL1蛋白的表达。裸鼠移植瘤实验检测敲低lncRNA XIST对GBC肿瘤生长的影响。结果GBC组织和细胞中miR-17-5p呈低表达,lncRNA XIST、FOSL1呈高表达。sh-XIST组细胞存活率、增殖数、划痕愈合率、侵袭数,Ki67、Cyclin D1、MMP-2、CD44表达水平低于sh-NC组、Ctrl组(P<0.05);sh-XIST+inhibitor-miR-17-5p组细胞存活率、增殖数、划痕愈合率、侵袭数及Ki67、Cyclin D1、MMP-2、CD44表达水平高于sh-XIST组、sh-XIST+inhibitor-NC组(P<0.05)。mimic-miR-17-5p组细胞存活率、增殖数、划痕愈合率、侵袭数及Ki67、Cyclin D1、MMP-2、CD44、FOSL1表达水平低于mimic-NC组、Ctrl组(P<0.05);mimic-miR-17-5p+OE-FOSL1组细胞存活率、增殖数、划痕愈合率、侵袭数及Ki67、Cyclin D1、MMP-2、CD44、FOSL1表达水平高于mimic-miR-17-5p组、mimic-miR-17-5p+OE-NC组(P<0.05)。lncRNA XIST可以靶向负调控miR-17-5p,而miR-17-5p可以靶向负调控FOSL1(P<0.05)。XIST敲低组裸鼠移植瘤体积、体质量,肿瘤FOSL1蛋白、lncRNA XIST表达水平低于阴性对照组,miR-17-5p表达水平高于阴性对照组(P<0.05)。结论lncRNA XIST通过调控miR-17-5p/FOSL1轴促进GBC细胞的增殖、迁移和侵袭。 展开更多
关键词 长链非编码RNA X染色体失活特异性转录本 微小RNA-17-5p FOS样抗原1 胆囊癌 增殖 迁移 侵袭
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LncRNA XIST调控miR-299-5p/CD36轴对结肠癌细胞增殖、凋亡及PD-1/PD-L1表达的影响 认领 引用
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作者 吴凡 张涛 +1 位作者 张子良 朱卫东 《联勤军事医学》 CAS 2026年第4期372-379,442,共8页
目的探讨长链非编码RNA X失活特异性转录本(long non-coding RNA X-inactive specific transcript,LncRNA XIST)调控微小RNA-299-5p(microRNA-299-5p,miR-299-5p)/分化簇36(cluster of differentiation 36,CD36)轴对结肠癌细胞增殖、凋... 目的探讨长链非编码RNA X失活特异性转录本(long non-coding RNA X-inactive specific transcript,LncRNA XIST)调控微小RNA-299-5p(microRNA-299-5p,miR-299-5p)/分化簇36(cluster of differentiation 36,CD36)轴对结肠癌细胞增殖、凋亡及程序性细胞死亡蛋白1(programmed cell death protein 1,PD-1)/程序性细胞死亡蛋白-配体1(programmed cell death protein-ligand 1,PD-L1)表达的影响。方法实时荧光定量聚合酶链式反应(real-time polymerase chain reaction,RT-PCR)检测结肠癌组织和细胞中LncRNA XIST、miR-299-5p、CD36和PD-L1 mRNA表达水平;验证miR-299-5p与LncRNA XIST和CD36的靶向关系。将HCT29细胞随机分为NC组、sh-NC组、sh-LncRNA XIST组、sh-LncRNA XIST+anti-NC组、sh-LncRNA XIST+anti-miR-299-5p组、sh-LncRNA XIST+pc-NC组,sh-LncRNA XIST+pc-CD36组;细胞计数试剂盒-8(cell counting kit-8,CCK-8)检测细胞活力;Transwell实验检测细胞迁移和侵袭能力;Hoechst333258染色检测细胞凋亡;蛋白免疫印迹法检测增殖细胞核抗原(proliferating cell nuclear antigen,PCNA)、CD36、PD-L1、活化的半胱氨酸天冬氨酸蛋白酶-3(cleaved cysteine-aspartic acid protease-3,cleaved caspase-3)和基质金属肽酶9(matrix metalloproteinase 9,MMP-9)蛋白表达水平。将上述各组细胞与CD8+T细胞共培养,台盼蓝染色检测CD8+T细胞活性;酶联免疫吸附试验(enzyme-linked immunosorbent assay,ELISA)检测共培养上清中PD-L1和干扰素-γ(interferon-γ,IFN-γ)水平。结果与癌旁组织比较,结肠癌组织中miR-299-5p mRNA表达水平降低,LncRNA XIST、CD36和PD-L1 mRNA表达水平升高(P均<0.05)。与NCM460细胞比较,结肠癌细胞系中miR-299-5p mRNA表达降低,LncRNA XIST、CD36和PD-L1 mRNA表达水平升高(P均<0.05)。miR-299-5p mimic+LncRNA XIST-WT双荧光素酶活性低于miR-NC+LncRNA XIST-WT(P<0.05),miR-299-5p mimic+CD36-WT双荧光素酶活性低于miR-NC+CD36-WT(P<0.05)。与NC组和sh-NC组比较,sh-LncRNA XIST组miR-299-5p mRNA表达水平、凋亡率、cleaved caspase-3蛋白表达水平、CD8+T细胞存活率、共培养上清IFN-γ水平升高;LncRNA XIST、CD36和PD-L1 mRNA表达水平,细胞活力,迁移和侵袭细胞数量,MMP-9、PCNA、PD-L1和CD36蛋白表达水平,共培养上清PD-L1水平降低(P均<0.05)。下调miR-299-5p表达和过表达CD36均可减弱沉默LncRNA XIST表达对HCT29细胞恶性生物学行为的抑制作用(P均<0.05)。结论沉默LncRNA XIST表达可能通过调控miR-299-5p/CD36轴来抑制结肠癌细胞增殖和免疫逃逸,促进细胞凋亡。 展开更多
关键词 长链非编码RNA X失活特异性转录本 微小RNA-299-5p/分化簇36轴 结肠癌 增殖 凋亡 程序性细胞死亡蛋白1 程序性细胞死亡蛋白-配体1
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血清lncRNA GAS5、miR-223-3p对帕金森病的早期诊断价值及其与病情严重程度的相关性分析 认领 引用 被引量：1
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作者 郝洁 刘昌佳 +1 位作者 闫昆 白雪娇 《检验医学与临床》 CAS 2025年第12期1655-1660,共6页
目的 探讨血清长链非编码RNA生长停滞特异性转录本5(lncRNA GAS5)、miR-223-3p对帕金森病(PD)的早期诊断价值及其与病情严重程度的相关性。方法 选取2023年6月至2024年6月该院收治的89例PD患者作为PD组,根据帕金森病评分量表(UPDRS)、Ho... 目的 探讨血清长链非编码RNA生长停滞特异性转录本5(lncRNA GAS5)、miR-223-3p对帕金森病(PD)的早期诊断价值及其与病情严重程度的相关性。方法 选取2023年6月至2024年6月该院收治的89例PD患者作为PD组,根据帕金森病评分量表(UPDRS)、Hoehn-Yahr分级量表评估患者的病情严重程度及分期。另选取同期该院89例健康体检者作为对照组。采用实时荧光定量反转录聚合酶链反应检测所有研究对象血清lncRNA GAS5、miR-223-3p水平。采用Pearson相关分析PD患者血清lncRNA GAS5水平与miR-223-3p水平的相关性;采用Spearman相关分析PD患者血清lncRNA GAS5水平、miR-223-3p水平与UPDRS评分、Hoehn-Yahr分级的相关性。采用多因素Logistic回归分析PD发生的影响因素。绘制受试者工作特征(ROC)曲线分析血清lncRNA GAS5、miR-223-3p对PD的诊断价值。结果 PD组有PD遗传病史患者占比高于对照组,差异有统计学意义(P<0.05)。PD组血清lncRNA GAS5水平低于对照组,血清miR-223-3p水平高于对照组,差异均有统计学意义(P<0.05)。轻度组、中度组、重度组血清lncRNA GAS5水平依次降低,血清miR-223-3p水平依次升高,差异均有统计学意义(P<0.05)。Pearson相关分析结果显示,PD患者血清lncRNA GAS5水平与血清miR-223-3p水平呈负相关(r=-0.616,P<0.001)。Spearman相关分析结果显示,PD患者血清lncRNA GAS5水平与UPDRS评分、Hoehn-Yahr分级均呈负相关(r_s=-0.687、-0.837,P<0.001);PD患者血清miR-223-3p水平与UPDRS评分、Hoehn-Yahr分级均呈正相关(r_s=0.606、0.795,P<0.001)。多因素Logistic回归分析结果显示,有PD遗传病史及血清miR-223-3p水平升高是PD发生的危险因素(P<0.05);血清lncRNA GAS5水平升高是PD发生的保护因素(P<0.05)。血清lncRNA GAS5、miR-223-3p联合诊断PD的曲线下面积(AUC)为0.940,明显高于二者单独诊断的AUC(0.827、0.823),差异均有统计学意义(P<0.05)。结论 PD患者血清lncRNA GAS5水平降低,miR-223-3p水平升高,均与PD的病情严重程度相关,二者联合检测对PD有较高的早期诊断价值。 展开更多
关键词 帕金森病 长链非编码RNA生长停滞特异性转录本5 微小RNA-223-3p 病情严重程度 早期诊断
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lncRNA GAS5基因多态性与多囊卵巢综合征发病风险的相关性研究 认领 引用
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作者 陆玉兰 庞晓霞 +2 位作者 陈兴鸿 韦玉霞 刘纯宏 《中国病理生理杂志》 CAS CSCD 北大核心 2025年第2期348-353,共6页
目的:研究长链非编码RNA(lncRNA)生长阻滞特异性转录物5(GAS5)基因多态性与多囊卵巢综合征(PCOS)发病的关联性。方法:选取2018年5月~2019年5月在广西右江民族医学院附属医院生殖医学中心确诊的236例PCOS患者作为病例组,同时选取同期性... 目的:研究长链非编码RNA(lncRNA)生长阻滞特异性转录物5(GAS5)基因多态性与多囊卵巢综合征(PCOS)发病的关联性。方法:选取2018年5月~2019年5月在广西右江民族医学院附属医院生殖医学中心确诊的236例PCOS患者作为病例组,同时选取同期性别、年龄相匹配的277例健康女性作为对照组,采用iMLDR单核苷酸多态性(SNP)分型方法检测GAS5基因rs145204276 I/D、rs55829688 C/T和rs6790 G/A位点基因型。采用logistic回归分析GAS5基因多态性与PCOS的相关性。结果:GAS5基因rs145204276 I/D位点多态性在对照组和PCOS组之间差异有统计学意义,logistic回归分析结果显示,与I/I基因型相比,I/D和D/D基因型以及显性模型I/D+D/D具有较低的PCOS发病风险[I/D vs I/I:OR(95%CI)=0.61(0.42,0.88),P=0.009;D/D vs I/I:OR(95%CI)=0.44(0.23,0.84),P=0.013;I/D+D/D vs I/I:OR(95%CI)=0.57(0.40,0.81),P=0.002];与I等位基因相比,D等位基因显著降低PCOS的发病风险[D vs I:OR(95%CI)=0.62(0.47,0.82),P=0.001]。rs55829688 C/T和rs6790 G/A位点多态性在对照组和PCOS组之间比较差异均无统计学意义(P>0.05)。单倍型联合分析显示D-T-A单倍型在对照组和PCOS组间的分布差异有统计学意义[OR(95%CI)=0.61(0.45,0.84),P=0.002]。结论:GAS5基因rs145204276 I/D位点多态性可能与PCOS遗传易感性相关,即携带D等位基因的个体可能具有较低的PCOS发病风险。 展开更多
关键词 多囊卵巢综合征 单核苷酸多态性 长链非编码RNA 生长阻滞特异性转录物5
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长链非编码RNA核富集转录本1对瘢痕成纤维细胞增殖、凋亡和迁移的影响 认领 引用
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作者 张彦峰 张慧敏 +1 位作者 何翔 郑屿萍 《中国组织工程研究》 CAS 北大核心 2025年第2期347-354,共8页
背景:已有研究阐明核富集转录本1(nuclear enriched abundant transcript 1,NEAT1)下调抑制了瘢痕成纤维细胞的进展,但具体机制尚不完全清楚。目的:探讨长链非编码RNA NEAT1调节miR-136-5p/泛素特异性蛋白酶4(ubiquitin specific protea... 背景:已有研究阐明核富集转录本1(nuclear enriched abundant transcript 1,NEAT1)下调抑制了瘢痕成纤维细胞的进展,但具体机制尚不完全清楚。目的:探讨长链非编码RNA NEAT1调节miR-136-5p/泛素特异性蛋白酶4(ubiquitin specific protease 4,USP4)轴对瘢痕成纤维细胞生物学行为的影响。方法:将瘢痕成纤维细胞分为5组:si-NC组、空白对照组、si-NEAT1组、si-NEAT1+miR-136-5p inhibitor组、si-NEAT1+inhibitor-NC组,qRT-PCR检测NEAT1、miR-136-5p表达;CCK-8法及EDU染色检测细胞增殖能力;流式细胞术检测细胞凋亡情况;划痕愈合实验检测细胞迁移情况;Western blot检测USP4、p27、Bax、基质金属蛋白酶9、α-平滑肌肌动蛋白、Ⅰ型胶原蛋白α1链蛋白表达;双荧光素酶实验检测NEAT1与miR-136-5p、miR-136-5p与USP4的关系。结果与结论:①与si-NC组比较,si-NEAT1组NEAT1表达、A450值、EDU阳性细胞百分比、划痕愈合率以及USP4、基质金属蛋白酶9、α-平滑肌肌动蛋白、Ⅰ型胶原蛋白α1链蛋白表达降低(P<0.05),miR-136-5p表达、细胞凋亡率及p27、Bax蛋白表达升高(P<0.05);②miR-136-5p inhibitor逆转了沉默NEAT1对瘢痕成纤维细胞生物学行为的影响;③miR-136-5p与NEAT1、miR-136-5p与USP4存在靶向调控关系。结果表明,沉默NEAT1可能通过调控miR-136-5p/USP4轴抑制瘢痕成纤维细胞的增殖和迁移,诱导其凋亡。 展开更多
关键词 长链非编码RNA核富集转录本1 miR-136-5p 泛素特异性蛋白酶4 瘢痕成纤维细胞 增殖
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