首页> 外文期刊>European review for medical and pharmacological sciences. >LncRNA BCAR4 promotes proliferation, invasion and metastasis of non-small cell lung cancer cells by affecting epithelial-mesenchymal transition
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LncRNA BCAR4 promotes proliferation, invasion and metastasis of non-small cell lung cancer cells by affecting epithelial-mesenchymal transition

机译:LncRNA BCAR4通过影响上皮-间质转化促进非小细胞肺癌细胞的增殖,侵袭和转移

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OBJECTIVE: Long non-coding RNAs (lncRNAs) play an important role in various cellular biological processes. It is also involved in the occurrence and development of the tumor. BCAR4 is reported to be highly expressed in breast cancer and promotes cell proliferation. However, the biological effects of BCAR4 in non-small cell lung cancer (NSCLC) remains unclear. PATIENTS AND METHODS: qRT-PCR was performed for detecting BCAR4 expression in 76 pairs of NSCLC tissues and corresponding cancer-adjacent tissues and 6 NSCLC cell lines. BCAR4 expression was knocked down, and its effects on NSCLC cell proliferation, cycle, apoptosis, invasion and metastasis were studied via MTT, clone formation, flow cytometry, TUNEL and Transwell assay. Metastatic tumor model of nude mice was established to investigate its effects on NSCLC cell metastasis. BCAR4 downstream target gene protein expression was detected using Western blotting and immunofluorescence assay. RESULTS: BCAR4 was higher in NSCLC tissues than that in cancer-adjacent tissues and was positively correlated with tumor size, clinical stage, and distant metastasis, suggesting that BCAR4 can be used as an independent predictor of prognosis. Results also showed that BCAR4 knockdown could inhibit tumor cell invasion, metastasis, and proliferation, induce cell cycle arrest and increase cell apoptosis. BCAR4 knockdown inhibits the metastasis and invasion of tumor cells via regulating Vimentin, N-cadherin and E-cadherin in Epithelial-Mesenchymal Transition (EMT). CONCLUSIONS: BCAR4 promotes the invasion and metastasis of NSCLC via regulating EMT and BCAR4/EMT interaction can be used as a new target for the diagnosis and therapeutics of NSCLC.
机译:目的:长非编码RNA(lncRNA)在各种细胞生物学过程中发挥重要作用。它也与肿瘤的发生和发展有关。据报道BCAR4在乳腺癌中高表达并促进细胞增殖。但是,BCAR4在非小细胞肺癌(NSCLC)中的生物学作用仍不清楚。病人与方法:采用qRT-PCR检测76对非小细胞肺癌组织及相应癌旁组织和6种非小细胞肺癌细胞系中BCAR4的表达。敲低BCAR4的表达,并通过MTT,克隆形成,流式细胞术,TUNEL和Transwell法研究其对NSCLC细胞增殖,周期,凋亡,侵袭和转移的影响。建立裸鼠转移性肿瘤模型,以研究其对NSCLC细胞转移的影响。使用蛋白质印迹和免疫荧光测定法检测BCAR4下游靶基因蛋白表达。结果:NSCLC组织中的BCAR4高于癌旁组织,与肿瘤的大小,临床分期和远处转移呈正相关,提示BCAR4可作为预后的独立预测指标。结果还表明,BCAR4敲低可以抑制肿瘤细胞的侵袭,转移和增殖,诱导细胞周期停滞并增加细胞凋亡。 BCAR4敲低通过调节上皮-间质转化(EMT)中的波形蛋白,N-钙粘着蛋白和E-钙粘着蛋白来抑制肿瘤细胞的转移和侵袭。结论:BCAR4通过调节EMT促进NSCLC的侵袭和转移,BCAR4 / EMT相互作用可作为NSCLC诊断和治疗的新靶点。

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