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转化生长因子-β1诱导的MALAT1上调通过上皮-间质转化促进哈萨克族食管鳞状细胞癌侵袭。

TGF-β1-Induced Upregulation of MALAT1 Promotes Kazakh's Esophageal Squamous Cell Carcinoma Invasion by EMT.

作者信息

Liu Qing, Zheng Shutao, Chen Yumei, Liu Tao, Han Xiujuan, Zhang Xiao, Shen Tongxue, Lu Xiaomei

机构信息

Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi, PR China.

State Key Laboratory of Pathogenesis, Prevention, Treatment of High Incidence Diseases in Central Asian, Xinjiang Uygur Autonomous Region, Urumqi, PR China.

出版信息

J Cancer. 2020 Oct 4;11(23):6892-6901. doi: 10.7150/jca.48426. eCollection 2020.

DOI:10.7150/jca.48426
PMID:33123280
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7592017/
Abstract

Transforming growth factor β1 (TGF-β1) plays an important role in tumor initiation and development by inducing epithelial-mesenchymal Transition (EMT). Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is a long noncoding RNA (lncRNA) that contributes to the invasion and metastasis of tumors, including esophageal squamous cell carcinoma (ESCC). The aim of the present study was to explore the underlying mechanisms implicated in EMT and to clarify whether TGF-β1 regulates MALAT1 expression, thereby promoting the invasion of ESCC. Expression of TGF-β1, MALAT1 and EMT-related markers, including E-cadherin and Vimentin, was detected in clinical samples of Kazakh's ESCC. The role of TGF-β1 in the regulation of MALAT1 in ESCC invasion was evaluated at the ESCC cell line level. High TGF-β1 expression was significantly associated with poor survival among patients with Kazakh's ESCC. Additionally, the expression of Vimentin was upregulated, and the expression of E-cadherin was downregulated and varied. The expression of MALAT1 positively correlated with the expression of TGF-β1 both and . Furthermore, knockdown of MALAT1 inhibited TGF-β1-induced EMT. Our data indicate that MALAT1 is heavily involved in EMT induced by TGF-β1. MALAT1 may be a therapeutic target in the suppression of metastasis and invasion of ESCC.

摘要

转化生长因子β1(TGF-β1)通过诱导上皮-间质转化(EMT)在肿瘤的起始和发展中发挥重要作用。转移相关的肺腺癌转录本1(MALAT1)是一种长链非编码RNA(lncRNA),它促进包括食管鳞状细胞癌(ESCC)在内的肿瘤的侵袭和转移。本研究的目的是探讨EMT的潜在机制,并阐明TGF-β1是否调节MALAT1的表达,从而促进ESCC的侵袭。在哈萨克族ESCC临床样本中检测TGF-β1、MALAT1以及EMT相关标志物(包括E-钙黏蛋白和波形蛋白)的表达。在ESCC细胞系水平评估TGF-β1在调节MALAT1对ESCC侵袭中的作用。哈萨克族ESCC患者中TGF-β1高表达与较差的生存率显著相关。此外,波形蛋白表达上调,E-钙黏蛋白表达下调且存在差异。MALAT1的表达与TGF-β1的表达在[此处原文缺失具体相关内容]均呈正相关。此外,敲低MALAT1可抑制TGF-β1诱导的EMT。我们的数据表明,MALAT1在很大程度上参与了TGF-β1诱导的EMT。MALAT1可能是抑制ESCC转移和侵袭的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/714e25a58eec/jcav11p6892g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/05cdb09f64b5/jcav11p6892g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/34a00cfd9c4b/jcav11p6892g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/c661cfb02d05/jcav11p6892g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/714e25a58eec/jcav11p6892g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/05cdb09f64b5/jcav11p6892g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/e966902977be/jcav11p6892g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/75fa56b659ef/jcav11p6892g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/933094b8bb58/jcav11p6892g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/34a00cfd9c4b/jcav11p6892g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/c661cfb02d05/jcav11p6892g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e444/7592017/714e25a58eec/jcav11p6892g007.jpg

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