miR-506 调控乳腺癌细胞系中的上皮间质转化。
miR-506 regulates epithelial mesenchymal transition in breast cancer cell lines.
机构信息
Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
出版信息
PLoS One. 2013 May 22;8(5):e64273. doi: 10.1371/journal.pone.0064273. Print 2013.
Epithelial-mesenchymal transition (EMT) is an important parameter related to breast cancer survival. Among several microRNAs predicted to target EMT-related genes, miR-506 is a novel miRNA found to be significantly related to breast cancer patient survival in a meta-analysis. miR-506 suppressed the expression of mesenchymal genes such as Vimentin, Snai2, and CD151 in MDA-MB-231 human breast cancer cell line. Moreover, NF-κB bound to the upstream promoter region of miR-506 to suppress transcription. Overexpression of miR-506 inhibited TGFβ-induced EMT and suppressed adhesion, invasion, and migration of MDA-MB-231 cells. From these results, we concluded that miR-506 plays a key role in the process of EMT through posttranslational control of EMT-related genes.
上皮-间充质转化（EMT）是与乳腺癌生存相关的一个重要参数。在几种被预测能靶向 EMT 相关基因的 microRNA 中，miR-506 是在荟萃分析中被发现与乳腺癌患者生存显著相关的一种新的 microRNA。miR-506 抑制了 MDA-MB-231 人乳腺癌细胞系中间充质基因如波形蛋白、Snai2 和 CD151 的表达。此外，NF-κB 与 miR-506 的上游启动子区域结合以抑制转录。miR-506 的过表达抑制了 TGFβ 诱导的 EMT，并抑制了 MDA-MB-231 细胞的黏附、侵袭和迁移。从这些结果中，我们得出结论，miR-506 通过 EMT 相关基因的翻译后调控在 EMT 过程中发挥关键作用。
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