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长链非编码RNA缺失通过激活STAT3/c-Myc/FAK信号通路抑制食管腺癌细胞增殖并诱导其凋亡。

LncRNA abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling.

作者信息

Su Wenmei, Guo Chunfang, Wang Lihui, Wang Zhuwen, Yang Xia, Niu Feiyu, Tzou Daniel, Yang Xiao, Huang Xiaobi, Wu Jiancong, Chen Xiaorao, Zou Lei, Yang Zhixiong, Chen Guoan

机构信息

Department of Oncology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.

Department of Surgery, University of Michigan, Ann Arbor, Ann Arbor, MI 48109, USA.

出版信息

Aging (Albany NY). 2019 Jul 10;11(13):4587-4596. doi: 10.18632/aging.102071.

DOI:10.18632/aging.102071
PMID:31291201
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6660029/
Abstract

Long non-coding RNAs (lncRNAs) have involved in human malignancies and played an important role in gene regulations. The dysregulation of lncRNA has been reported in several cancers. However, the role of in esophageal adenocarcinoma (EAC) is poorly understood. Loss of function approaches were used to investigate the biological role of in EAC cells. The effects of on cell proliferation were evaluated by WST-1 and colony formation assays. The effects of on cell migration and invasion were examined using transwell assays. QRT-PCR and Western blot were used to evaluate the mRNA and protein expression of related genes. In this study, abrogation of inhibited cell proliferation, colony formation, invasion and migration in EAC 3 cell lines (OE33, OE19 and FLO-1). Mechanistically, silencing decreased the expression of STAT3/c-Myc/p-FAK proteins and induced apoptosis in EAC cell lines. These results delineate a novel mechanism of in EAC, and may provide potential targets by developing lncRNA-based therapies for EAC.

摘要

长链非编码RNA(lncRNAs)参与人类恶性肿瘤的发生,并在基因调控中发挥重要作用。lncRNA的失调已在多种癌症中被报道。然而,其在食管腺癌(EAC)中的作用仍知之甚少。采用功能缺失方法研究其在EAC细胞中的生物学作用。通过WST-1和集落形成试验评估其对细胞增殖的影响。使用Transwell试验检测其对细胞迁移和侵袭的影响。采用QRT-PCR和蛋白质免疫印迹法评估相关基因的mRNA和蛋白质表达。在本研究中,敲除该lncRNA可抑制EAC 3种细胞系(OE33、OE19和FLO-1)的细胞增殖、集落形成、侵袭和迁移。机制上,该lncRNA沉默可降低EAC细胞系中STAT3/c-Myc/p-FAK蛋白的表达并诱导细胞凋亡。这些结果揭示了该lncRNA在EAC中的一种新机制,并可能通过开发基于lncRNA的EAC治疗方法提供潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/c42975ae8106/aging-11-102071-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/ef5b61546b4e/aging-11-102071-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/ebe36ee3875d/aging-11-102071-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/5ae0d066986e/aging-11-102071-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/98f25596ef28/aging-11-102071-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/77ba9fb12ccc/aging-11-102071-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/c42975ae8106/aging-11-102071-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/ef5b61546b4e/aging-11-102071-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/ebe36ee3875d/aging-11-102071-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/5ae0d066986e/aging-11-102071-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/98f25596ef28/aging-11-102071-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/77ba9fb12ccc/aging-11-102071-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/007e/6660029/c42975ae8106/aging-11-102071-g006.jpg

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