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长链非编码RNA XIST通过调控miR-101/EZH2促进食管鳞状细胞癌的恶性进展。

Long noncoding RNA XIST promotes malignancies of esophageal squamous cell carcinoma via regulation of miR-101/EZH2.

作者信息

Wu Xiaoliang, Dinglin Xiaoxiao, Wang Xing, Luo Wen, Shen Qi, Li Yong, Gu Ling, Zhou Qianghua, Zhu Haotu, Li Yanjie, Tan Chaodi, Yang Xianzi, Zhang Zhenfeng

机构信息

Department of Oncology, Guizhou Provincial People's Hospital, Guiyang, China.

State Key Laboratory of Oncology in South China & Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.

出版信息

Oncotarget. 2017 Jun 27;8(44):76015-76028. doi: 10.18632/oncotarget.18638. eCollection 2017 Sep 29.

DOI:10.18632/oncotarget.18638
PMID:29100288
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5652682/
Abstract

The long non-coding RNA XIST is a long non-coding RNA that associates with polycomb repressive complex 2 to regulate X-chromosome inactivation in female mammals. The biological roles as well as the underlying mechanisms of XIST in esophageal squamous cell carcinoma remained yet to be solved. Our data indicated that XIST was significantly upregulated in esophageal squamous cancerous tissues and cancer cell lines, as compared with that in the corresponding non-cancerous tissues and immortalized normal squamous epithelial cells. High XIST expression predicted poor prognosis of esophageal squamous cancer patients. Lentivirus mediated knockdown of XIST inhibited proliferation, migration and invasion of esophageal squamous cancer cells and suppressed tumor growth . Knockdown of XIST resulted in elevated expression of miR-101 and decreased expression of EZH2. Further analysis showed that XIST functioned as the competitive endogenous RNA of miR-101 to regulate EZH2 expression. Moreover, enforced expression of EZH2 significantly attenuated the anti-proliferation activity upon XIST knockdown. Conclusively, XIST plays an important role in malignant progression of ESCC via modulation of miR-101/EZH2 axis.

摘要

长链非编码RNA XIST是一种长链非编码RNA，它与多梳抑制复合物2结合，以调节雌性哺乳动物的X染色体失活。XIST在食管鳞状细胞癌中的生物学作用及其潜在机制仍有待解决。我们的数据表明，与相应的非癌组织和永生化正常鳞状上皮细胞相比，XIST在食管鳞状癌组织和癌细胞系中显著上调。XIST高表达预示食管鳞状癌患者预后不良。慢病毒介导的XIST敲低抑制了食管鳞状癌细胞的增殖、迁移和侵袭，并抑制了肿瘤生长。XIST敲低导致miR-101表达升高和EZH2表达降低。进一步分析表明，XIST作为miR-101的竞争性内源性RNA来调节EZH2表达。此外，EZH2的强制表达显著减弱了XIST敲低后的抗增殖活性。总之，XIST通过调节miR-101/EZH2轴在食管鳞状细胞癌的恶性进展中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/01380a83072d/oncotarget-08-76015-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/863613617655/oncotarget-08-76015-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/0a4872ee14c0/oncotarget-08-76015-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/6376a7e868f4/oncotarget-08-76015-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/0ac381aa16ab/oncotarget-08-76015-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/c963dc5a81cb/oncotarget-08-76015-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/e6578d1f998e/oncotarget-08-76015-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/01380a83072d/oncotarget-08-76015-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/863613617655/oncotarget-08-76015-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/0a4872ee14c0/oncotarget-08-76015-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/6376a7e868f4/oncotarget-08-76015-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/0ac381aa16ab/oncotarget-08-76015-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/c963dc5a81cb/oncotarget-08-76015-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/e6578d1f998e/oncotarget-08-76015-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f99/5652682/01380a83072d/oncotarget-08-76015-g007.jpg

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