Department of General Surgery, Changji Huizu People's Hospital of Xinjiang, Xinjiang, China.
Eur Rev Med Pharmacol Sci. 2018 Dec;22(23):8383-8390. doi: 10.26355/eurrev_201812_16536.
Breast cancer is one of the most common malignancies worldwide. MicroRNAs (MiRNAs) have been identified to influence cell behaviors through epigenetic post-transcriptional gene regulation. Therefore, the aim of this study was to determine the role of miR-3196 in the proliferation and apoptosis of breast cancer.
Human breast cancer cell lines (MCF-7 and MDA-MB-231) were obtained and cultured. The expression level of miR-3196 in breast cancer tissues was detected using Real Time-Polymerase Chain Reaction (RT-PCR). The effects of miR-3196 on the proliferation and apoptosis of breast cancer cells were analyzed by cell counting kit-8 (CCK-8) assay and TUNEL assay, respectively. In addition, the interaction between miR-3196 expression and erb-b2 receptor tyrosine kinase 3 (ERBB3) expression, as well as the mechanism of miR-3196 regulating ERBB3 in breast cancer, were also addressed by RT-PCR, Western blot, and luciferase reporter gene assay.
MiR-3196 was lowly expressed in breast cancer tissues. Overexpression of miR-3196 could repress the proliferation and induce the apoptosis of breast cancer cells via targeting the 3'UTR of ERBB3.
Our findings provide novel insights into the role of miR-3196 in breast cell proliferation and apoptosis. Meanwhile, this study suggests that miR-3196 can serve as a potential biomarker and therapeutic target for breast cancer.
乳腺癌是全球最常见的恶性肿瘤之一。microRNAs（miRNAs）已被鉴定通过表观遗传转录后基因调控影响细胞行为。因此，本研究旨在确定 miR-3196 在乳腺癌增殖和凋亡中的作用。
获取并培养人乳腺癌细胞系（MCF-7 和 MDA-MB-231）。采用实时聚合酶链反应（RT-PCR）检测乳腺癌组织中 miR-3196 的表达水平。通过细胞计数试剂盒-8（CCK-8）测定和 TUNEL 测定分别分析 miR-3196 对乳腺癌细胞增殖和凋亡的影响。此外，通过 RT-PCR、Western blot 和荧光素酶报告基因测定研究了 miR-3196 表达与 erb-b2 受体酪氨酸激酶 3（ERBB3）表达之间的相互作用以及 miR-3196 调节乳腺癌中 ERBB3 的机制。
miR-3196 在乳腺癌组织中低表达。miR-3196 的过表达可以通过靶向 ERBB3 的 3'UTR 抑制乳腺癌细胞的增殖并诱导其凋亡。
本研究结果为 miR-3196 在乳腺癌细胞增殖和凋亡中的作用提供了新的见解。同时，本研究提示 miR-3196 可以作为乳腺癌的潜在生物标志物和治疗靶点。
