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CEP131基因敲低通过抑制非小细胞肺癌中的ERK和AKT信号通路来抑制细胞增殖。

CEP131 knockdown inhibits cell proliferation by inhibiting the ERK and AKT signaling pathways in non-small cell lung cancer.

作者信息

Wang Junying, Yang Xiaoping, Han Shixin, Zhang Lizhi

机构信息

Department of Pathology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, P.R. China.

Department of Anesthesiology, Dalian Obstetrics and Gynecology Hospital, Dalian, Liaoning 116033, P.R. China.

出版信息

Oncol Lett. 2020 Apr;19(4):3145-3152. doi: 10.3892/ol.2020.11411. Epub 2020 Feb 19.

DOI:10.3892/ol.2020.11411
PMID:32218865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7068694/
Abstract

Disrupted centrosome-associated family protein expression can result in the detrimental duplication of centrosomes, causing genomic instability and subsequent carcinogenesis. Limited research has demonstrated that centrosomal protein 131 (CEP131) exhibits oncogenic activity in osteosarcoma, hepatocellular carcinoma and breast cancer. The present study demonstrated that there is an association between CEP131 expression and advanced Tumor-Node-Metastasis stage (P=0.016), and positive regional lymph node metastasis (P=0.023) in 91 cases of non-small cell lung cancer. A549 and SPC-A-1 cells, with moderate expression levels of CEP131, were selected as representative cell lines. The results indicated that downregulation of CEP131 induced G1/S cell cycle arrest, inhibition of cyclins D1/E and cyclin-dependent kinases 2/4/6, and induction of inhibitory p21/p27, all of which are regulated by ERK and AKT signaling, suggesting that CEP131 exhibits potential as a novel target in the treatment of lung cancer.

摘要

中心体相关家族蛋白表达紊乱可导致中心体有害复制，引发基因组不稳定及随后的致癌作用。有限的研究表明，中心体蛋白131（CEP131）在骨肉瘤、肝细胞癌和乳腺癌中表现出致癌活性。本研究表明，在91例非小细胞肺癌中，CEP131表达与肿瘤-淋巴结-转移（TNM）晚期（P=0.016）及区域淋巴结转移阳性（P=0.023）之间存在关联。选择CEP131表达水平中等的A549和SPC-A-1细胞作为代表性细胞系。结果表明，CEP131的下调诱导G1/S期细胞周期阻滞，抑制细胞周期蛋白D1/E和细胞周期蛋白依赖性激酶2/4/6，并诱导抑制性p21/p27，所有这些均受ERK和AKT信号通路调控，提示CEP131有望成为肺癌治疗的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a2f/7068694/13850ae94f81/ol-19-04-3145-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a2f/7068694/10a0510edb18/ol-19-04-3145-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a2f/7068694/c8f5332d06e5/ol-19-04-3145-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a2f/7068694/41a84e7e5995/ol-19-04-3145-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a2f/7068694/13850ae94f81/ol-19-04-3145-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a2f/7068694/10a0510edb18/ol-19-04-3145-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a2f/7068694/c8f5332d06e5/ol-19-04-3145-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a2f/7068694/41a84e7e5995/ol-19-04-3145-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a2f/7068694/13850ae94f81/ol-19-04-3145-g03.jpg

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