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长链非编码RNA OECC通过PI3K/Akt/mTOR信号通路促进人肺癌细胞的增殖和转移。

Long non-coding RNA OECC promotes cell proliferation and metastasis through the PI3K/Akt/mTOR signaling pathway in human lung cancer.

作者信息

Zou Yimin, Zhang Bin, Mao Yanxiong, Zhang Hao, Hong Wei

机构信息

Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China.

Guangzhou Medical University-Guangzhou Institute of Biomedicine and Health Joint School of Life Sciences, Guangzhou Medical University, Guangzhou, Guangdong 510030, P.R. China.

出版信息

Oncol Lett. 2019 Sep;18(3):3017-3024. doi: 10.3892/ol.2019.10644. Epub 2019 Jul 22.

DOI:10.3892/ol.2019.10644
PMID:31452780
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6704322/
Abstract

Lung cancer is one of the most common malignancies worldwide; however, its detailed molecular mechanism remains largely unknown. Long non-coding RNAs (lncRNAs) have been identified to serve critical roles in tumorigenesis. The aim of the present study was to investigate the role of a newly identified lncRNA, overexpressed in colorectal cancer (OECC), in human lung cancer. It was initially revealed that the relative transcript level of OECC was highly upregulated in clinical human lung cancer tissues as well as in cultured lung cancer cells. Knockdown of OECC with specific short hairpin RNAs in lung cancer cell lines A549 and 95D inhibited colony formation and cell viability, as evidenced using colony formation assays and cell proliferation assays. Furthermore, depletion of OECC in A549 and 95D cells suppressed migration and invasion, which was verified using Transwell assays. RNA-sequence analysis suggested that the phosphoinositide 3-kinase/protein kinase B (Akt)/mammalian target of rapamycin signaling pathway was positively regulated by OECC in lung cancer cells A549. In addition, overexpression of Akt in OECC-depleted A549 and 95D cells reversed the suppression of proliferation and migration caused by OECC depletion. The results of the present study identified lncRNA OECC as a novel regulator of lung cancer progression and provided new clues for the clinical treatment of lung cancer.

摘要

肺癌是全球最常见的恶性肿瘤之一;然而,其详细的分子机制仍 largely 未知。长链非编码 RNA(lncRNAs)已被确定在肿瘤发生中起关键作用。本研究的目的是调查一种新发现的在结直肠癌中过表达(OECC)的 lncRNA 在人类肺癌中的作用。最初发现,OECC 的相对转录水平在临床人类肺癌组织以及培养的肺癌细胞中高度上调。在肺癌细胞系 A549 和 95D 中用特异性短发夹 RNA 敲低 OECC 可抑制集落形成和细胞活力,集落形成试验和细胞增殖试验证明了这一点。此外,在 A549 和 95D 细胞中耗尽 OECC 可抑制迁移和侵袭,Transwell 试验验证了这一点。RNA 序列分析表明,在肺癌细胞 A549 中,磷酸肌醇 3 - 激酶/蛋白激酶 B(Akt)/雷帕霉素哺乳动物靶标信号通路受到 OECC 的正向调节。此外,在 OECC 耗尽的 A549 和 95D 细胞中过表达 Akt 可逆转 OECC 耗尽引起的增殖和迁移抑制。本研究结果确定 lncRNA OECC 是肺癌进展的一种新型调节因子,并为肺癌的临床治疗提供了新线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/7a6dfbdd419a/ol-18-03-3017-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/bc8bebc5341f/ol-18-03-3017-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/9020380d62fa/ol-18-03-3017-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/28d1861283f5/ol-18-03-3017-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/0bea9b4a2117/ol-18-03-3017-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/7a6dfbdd419a/ol-18-03-3017-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/bc8bebc5341f/ol-18-03-3017-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/9020380d62fa/ol-18-03-3017-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/28d1861283f5/ol-18-03-3017-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/0bea9b4a2117/ol-18-03-3017-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc9/6704322/7a6dfbdd419a/ol-18-03-3017-g04.jpg

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