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miR-143-3p通过靶向integrinβ1抑制肝癌进展
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作者 李丽坤 邸雅南 +1 位作者 陈帝 张晶 《中国组织化学与细胞化学杂志》 CAS CSCD 2023年第5期480-488,共9页
目的探讨肝癌中miR-143-3p的表达及其对肝癌细胞恶性生物学行为的影响,并分析潜在的机制。方法收集肝癌组织,用RT-qPCR和Western blot法分别检测miR-143-3p和integrinβ1的表达。体外培养肝癌细胞,并用miR-143-3p mimics转染后,用XTT和... 目的探讨肝癌中miR-143-3p的表达及其对肝癌细胞恶性生物学行为的影响,并分析潜在的机制。方法收集肝癌组织,用RT-qPCR和Western blot法分别检测miR-143-3p和integrinβ1的表达。体外培养肝癌细胞,并用miR-143-3p mimics转染后,用XTT和EDU法检测过表达miR-143-3p对细胞增殖活力的影响,用Transwell法检测过表达miR-143-3p对细胞迁移与侵袭的影响,Western blot法检测过表达miR-143-3p对integrinβ1表达的影响。用荧光素酶活性法检测miR-143-3p与integrinβ1的靶向关系。用XTT、EdU和Transwell法检测过表达integrinβ1对已转染miR-143-3p mimics的肝癌细胞增殖、迁移与侵袭的影响。结果与癌旁正常组织比较,肝癌组织中miR-143-3p表达降低,integrinβ1表达升高,且二者均随疾病分期进展进一步降低或增高。过表达miR-143-3p能抑制肝癌细胞增殖、迁移和侵袭,并能下调integrinβ1表达。过表达integrinβ1能逆转miR-143-3p对肝癌细胞的抑制作用。integrinβ1为miR-143-3p的靶点。结论miR-143-3p在肝癌中表达下调,而上调miR-143-3p能通过靶向integrinβ1抑制肝癌细胞增殖、迁移与侵袭。 展开更多
关键词 miR-143-3p 肝癌 integrinΒ1 增殖 迁移 侵袭
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Basic Study Long non-coding RNA TP73-AS1 promotes pancreatic cancer growth and metastasis through miRNA-128-3p/GOLM1 axis 被引量:3
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作者 Bin Wang Xing Sun +2 位作者 Ke-Jian Huang Li-Sheng Zhou Zheng-Jun Qiu 《World Journal of Gastroenterology》 SCIE CAS 2021年第17期1993-2014,共22页
BACKGROUND Previous studies have suggested that long non-coding RNAs(lncRNA)TP73-AS1 is significantly upregulated in several cancers.However,the biological role and clinical significance of TP73-AS1 in pancreatic canc... BACKGROUND Previous studies have suggested that long non-coding RNAs(lncRNA)TP73-AS1 is significantly upregulated in several cancers.However,the biological role and clinical significance of TP73-AS1 in pancreatic cancer(PC)remain unclear.AIM To investigate the role of TP73-AS1 in the growth and metastasis of PC.METHODS The expression of lncRNA TP73-AS1,miR-128-3p,and GOLM1 in PC tissues and cells was detected by quantitative real-time polymerase chain reaction.The bioinformatics prediction software ENCORI was used to predict the putative binding sites of miR-128-3p.The regulatory roles of TP73-AS1 and miR-128-3p in cell proliferation,migration,and invasion abilities were verified by Cell Counting Kit-8,wound-healing,and transwell assays,as well as flow cytometry and Western blot analysis.The interactions among TP73-AS1,miR-128-3p,and GOLM1 were explored by bioinformatics prediction,luciferase assay,and Western blot.RESULTS The expression of TP73-AS1 and miRNA-128-3p was dysregulated in PC tissues and cells.High TP73-AS1 expression was correlated with a poor prognosis.TP73-AS1 silencing inhibited PC cell proliferation,migration,and invasion in vitro as well as suppressed tumor growth in vivo.Mechanistically,TP73-AS1 was validated to promote PC progression through GOLM1 upregulation by competitively binding to miR-128-3p.CONCLUSION Our results demonstrated that TP73-AS1 promotes PC progression by regulating the miR-128-3p/GOLM1 axis,which might provide a potential treatment strategy for patients with PC. 展开更多
关键词 Pancreatic cancer Long non-coding RNA TP73-AS1 miR-128-3p GOLM1
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Lanthanides-Induced Cellular Signal Transduction: Implications in Pathogenesis of Fibrosis
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作者 HE Xia GUO Yuting +2 位作者 DONG Faqing WANG Kui YU Siwang 《矿物学报》 CAS CSCD 北大核心 2013年第S1期34-34,共1页
With the extensive mining and application of lanthanides in China and worldwide, the potential impact of lanthanides on human health is gaining increasing attentions. The recent etiological association of gadolinium-b... With the extensive mining and application of lanthanides in China and worldwide, the potential impact of lanthanides on human health is gaining increasing attentions. The recent etiological association of gadolinium-based contrast agents with nephrogenic systemic fibrosis (NSF) evoked widespread concerns regarding the safety issue of lanthanides. The elucidation of the cellular biological effects of and the signalling cascade induced lanthanides is essential for proper evaluation of their health impacts. 展开更多
关键词 GADOLINIUM LANTHANUM nephrogenic SYSTEMIC FIBROSIS HEK 293 Cell cycle EGFR PI3K/Akt MAPK TGFΒ-1 integrinαVβ1
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