miR-934 promotes breast cancer metastasis by regulation of PTEN and epithelial–mesenchymal transition

转移 基因敲除 上皮-间质转换 癌症研究 生物 小RNA PTEN公司 下调和上调 乳腺癌 癌症 免疫印迹 细胞培养 PI3K/AKT/mTOR通路 细胞生物学 信号转导 基因 生物化学 遗传学
作者
Yexia Lu,Xiuxiu Hu,Xueyi Yang
出处
期刊:Tissue & Cell [Elsevier BV]
卷期号:71: 101581-101581 被引量:11
标识
DOI:10.1016/j.tice.2021.101581
摘要

Breast cancer (BC) is the most commonly diagnosed malignancy and the leading cause of cancer-related mortality among females. Over 90 % of the cases of death in BC patients are attributed to tumor cell metastasis. Therefore, it is urgently needed to investigate the molecular mechanisms of BC metastasis. The expression of miRNA in BC was evaluated by qRT-PCR and bioinformatics analysis. Clone formation, EdU assays, and subcutaneous xenograft model were used to test the growth of BC cells. Wound healing, transwell assays, and lung-metastasis model were used to explore the effect of miR-934 knockdown on cell metastasis. The miR-934 targets in BC were identified through bioinformatics analysis and luciferase reporter assays. The expression of protein was tested by western blot. The binding of mRNA and RNA-binding-protein was verified using RIP assays. miR-934 expression was significantly elevated in BC tissues, especially in those with lymph node metastasis and associated with poor patient prognosis. Experiments in vitro and in vivo showed that that upregulated miR-934 was not necessarily required for the growth of BC cells. However, miR-934 knockdown significantly inhibited the migration and invasion abilities of BC cells. Moreover, PTEN as identified as the direct target of miR-934 in BC, and miR-934 could promote BC cell metastasis by regulation of PTEN and epithelial-mesenchymal transition (EMT). Our results suggested that targeting miR-934 may be a practical treatment for BC cell metastasis.
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