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miR-23a 通过靶向肺癌细胞中的 E-钙黏蛋白调节 TGF-β诱导的上皮-间充质转化。

MiR-23a regulates TGF-β-induced epithelial-mesenchymal transition by targeting E-cadherin in lung cancer cells.

机构信息

Department of Internal Medicine, Division of Pulmonary Medicine/Infection and Oncology, Nippon Medical School, Tokyo 113-8603, Japan.

出版信息

Int J Oncol. 2012 Sep;41(3):869-75. doi: 10.3892/ijo.2012.1535. Epub 2012 Jun 28.

DOI:10.3892/ijo.2012.1535
PMID:22752005
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3582905/
Abstract

Transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition (EMT) has been shown to be related to the pathogenesis of various diseases including lung cancer. Recently, microRNAs (miRNA) have been recognized as a new class of genes involved in human tumorigenesis. MiR-23a/24/27a is a miRNA cluster located in chromosome 19p13.12, which can function as an oncogene in several human cancers. In this study, we analyzed miR-23a/24/27a expression in 10 non-small cell cancer (NSCLC) cell lines by real-time PCR analysis. Correlation between expression of these miRNAs and TGF-β/Smad signaling was evaluated. We found that miR-23a could be regulated by TGF-β1 in a Smad-dependent manner in A549 lung adenocarcinoma cells showing the EMT phenomenon. Knockdown of miR-23a partially restored E-cadherin expression under conditions of TGF-β1 stimulation. In contrast, overexpression of miR-23a could suppress E-cadherin expression and stimulate EMT. Furthermore, A549 cells with overexpressed miR-23a were more resistant to gefitinib compared to the parental cells. These findings suggest that miR-23a regulates TGF-β-induced EMT by targeting E-cadherin in lung cancer cells and may be useful as a new therapeutic target in NSCLC.

摘要

转化生长因子-β（TGF-β）诱导的上皮-间充质转化（EMT）已被证明与各种疾病的发病机制有关，包括肺癌。最近，microRNAs（miRNA）已被认为是参与人类肿瘤发生的一类新的基因。miR-23a/24/27a 是位于 19p13.12 染色体上的 miRNA 簇，可在几种人类癌症中作为癌基因发挥作用。在本研究中，我们通过实时 PCR 分析分析了 10 种非小细胞癌（NSCLC）细胞系中 miR-23a/24/27a 的表达。评估了这些 miRNA 的表达与 TGF-β/Smad 信号之间的相关性。我们发现，在具有 EMT 现象的 A549 肺腺癌细胞中，miR-23a 可以通过 TGF-β1 以 Smad 依赖性方式进行调节。在 TGF-β1 刺激下，miR-23a 的敲低部分恢复了 E-钙粘蛋白的表达。相比之下，miR-23a 的过表达可抑制 E-钙粘蛋白的表达并刺激 EMT。此外，与亲本细胞相比，过表达 miR-23a 的 A549 细胞对吉非替尼更具抗性。这些发现表明，miR-23a 通过靶向肺癌细胞中的 E-钙粘蛋白来调节 TGF-β 诱导的 EMT，并可能作为 NSCLC 的新治疗靶点有用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c69/3582905/e668f52b0778/IJO-41-03-0869-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c69/3582905/b41060821953/IJO-41-03-0869-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c69/3582905/612a4bbed52b/IJO-41-03-0869-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c69/3582905/84f2b111ff99/IJO-41-03-0869-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c69/3582905/e668f52b0778/IJO-41-03-0869-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c69/3582905/b41060821953/IJO-41-03-0869-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c69/3582905/612a4bbed52b/IJO-41-03-0869-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c69/3582905/84f2b111ff99/IJO-41-03-0869-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c69/3582905/e668f52b0778/IJO-41-03-0869-g04.jpg

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