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首页> 外文期刊>European review for medical and pharmacological sciences. >MiR-508-3p inhibits cell invasion and epithelial-mesenchymal transition by targeting ZEB1 in triple-negative breast cancer
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MiR-508-3p inhibits cell invasion and epithelial-mesenchymal transition by targeting ZEB1 in triple-negative breast cancer

机译:MiR-508-3p通过靶向ZEB1抑制三阴性乳腺癌中的细胞侵袭和上皮-间质转化

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OBJECTIVE: Recently, studies have identified that microRNAs (miRNAs) are novel regulators for gene expression in tumor progression including breast cancer. The aim of the study is to investigate the clinical significance and underlying functions between miR-508-3p expression and triple-negative breast cancer (TNBC) development. PATIENTS AND METHODS: Quantitative Real-time PCR (QRT-PCR) was performed to determine the expression of miR-508-3p in 54 pairs of TNBC specimens and adjacent non-tumor tissues. The association between miR-508-3p expression and clinicopathological factors was assessed using x2-test. Transwell invasion assays were used to assess cell invasion ability. Luciferase reporter assay, Western blot analyses and qRT-PCR were performed to demonstrate ZEB1 was a direct target of miR-508-3p. RESULTS: We demonstrated that miR-508-3p expression was remarkably decreased in TNBC tissues and cells. Lower miR-508-3p expression significantly associated with lymph node metastasis and distant metastasis in TNBC patients (p 0.05). Ectopic expression of miR-508-3p significantly suppressed cell invasion ability of TNBC. MiR-508-3p overexpression suppressed cell epithelial-mesenchymal transition (EMT) phenomenon of TNBC by upregulating E-cadherin expression, but downregulating Vimentin expression. In addition, we revealed that ZEB1 was a direct target of miR-508-3p in TNBC cells. MiR-508-3p significantly suppressed cell EMT process by regulating ZEB1 expression. CONCLUSIONS: We found that miR-508-3p may be a potential therapeutic target of TNBC.
机译:目的:最近,研究发现微RNA(miRNA)是在包括乳腺癌在内的肿瘤进展中表达基因的新型调节剂。该研究的目的是研究miR-508-3p表达与三阴性乳腺癌(TNBC)发育之间的临床意义和潜在功能。病人和方法:进行实时定量PCR(QRT-PCR)以确定miR-508-3p在54对TNBC标本和邻近的非肿瘤组织中的表达。使用x2检验评估了miR-508-3p表达与临床病理因素之间的关联。使用Transwell侵袭测定法评估细胞侵袭能力。进行荧光素酶报告基因测定,Western印迹分析和qRT-PCR证明ZEB1是miR-508-3p的直接靶标。结果:我们证明在TNBC组织和细胞中miR-508-3p表达显着降低。较低的miR-508-3p表达与TNBC患者的淋巴结转移和远处转移显着相关(p <0.05)。 miR-508-3p的异位表达显着抑制了TNBC的细胞侵袭能力。 MiR-508-3p过表达通过上调E-钙黏着蛋白表达,但下调波形蛋白表达来抑制TNBC的细胞上皮-间质转化(EMT)现象。此外,我们发现ZEB1是TNBC细胞中miR-508-3p的直接靶标。 MiR-508-3p通过调节ZEB1表达来显着抑制细胞EMT过程。结论:我们发现miR-508-3p可能是TNBC的潜在治疗靶标。

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