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miR-3196 的过表达通过靶向 ERBB3 抑制乳腺癌细胞增殖并诱导细胞凋亡。

Overexpression of miR-3196 suppresses cell proliferation and induces cell apoptosis through targeting ERBB3 in breast cancer.

机构信息

Department of General Surgery, Changji Huizu People's Hospital of Xinjiang, Xinjiang, China.

出版信息

Eur Rev Med Pharmacol Sci. 2018 Dec;22(23):8383-8390. doi: 10.26355/eurrev_201812_16536.

Abstract

OBJECTIVE

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.

MATERIALS AND METHODS

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.

RESULTS

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.

CONCLUSIONS

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.

摘要

目的

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。

材料与方法

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。

结果

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。

结论

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。

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