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Knockdown of microRNA-29a regulates the expression of apoptosis-related genes in MCF-7 breast carcinoma cells

机译:抑制microRNA-29a调节MCF-7乳腺癌细胞凋亡相关基因的表达

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摘要

MicroRNA (miR), as non-coding small RNA, are key regulators of cancer-related biological cell processes and contribute to tumor growth through regulation of groups of pro- and anti-apoptotic genes. The present study aimed to investigate the effects of miR-29a on the expression of genes involved in apoptosis, including p21, B-cell lymphoma 2 (BCL-2), p53 and survivin. The MCF-7 breast cancer cell line was transfected with anti-miR-29a and treated with Taxol in subdivided treatment groups including: Scramble; anti-miR-29a; anti-miR-29a + Taxol; Taxol; and control. Expression levels of p21, BCL-2, p53 and survivin were evaluated using reverse transcription-quantitative polymerase chain reaction. miR-29a knockdown resulted in p21 and p53 upregulation and a decrease in survivin expression. These results indicated that miR-29a inhibition regulates apoptosis. The present data suggested that miR-29a inhibition may be a promising strategy for the induction of apoptosis of tumor cells.
机译:作为非编码小RNA的MicroRNA(miR)是与癌症相关的生物细胞过程的关键调节剂,并通过调节促凋亡和促凋亡基因组来促进肿瘤生长。本研究旨在研究miR-29a对涉及凋亡的基因表达的影响,包括p21,B细胞淋巴瘤2(BCL-2),p53和survivin。在细分的治疗组中,将MCF-7乳腺癌细胞系用抗miR-29a转染并用紫杉醇处理。抗miR-29a;抗miR-29a +紫杉醇;紫杉醇;和控制。使用逆转录定量聚合酶链反应评估p21,BCL-2,p53和survivin的表达水平。 miR-29a敲低导致p21和p53上调以及survivin表达下降。这些结果表明miR-29a抑制调节细胞凋亡。目前的数据表明,miR-29a抑制可能是诱导肿瘤细胞凋亡的一种有前途的策略。

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