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MORF4L1通过增加鼻咽癌中p21和E-钙黏蛋白的表达来抑制细胞增殖、迁移和侵袭。

MORF4L1 suppresses cell proliferation, migration and invasion by increasing p21 and E-cadherin expression in nasopharyngeal carcinoma.

作者信息

Sang Yi, Zhang Ruhua, Sun Longhua, Chen Kaddie Kwok, Li Si-Wei, Xiong Longxin, Peng Yongjian, Zeng Lei, Huang Guofu

机构信息

Nanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, The Third Affiliated Hospital, Nanchang University, Nanchang, Jiangxi 330008, P.R. China.

State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong 510060, P.R. China.

出版信息

Oncol Lett. 2019 Jan;17(1):294-302. doi: 10.3892/ol.2018.9588. Epub 2018 Oct 16.

DOI:10.3892/ol.2018.9588
PMID:30655767
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6313188/
Abstract

Mortality factor 4-like 1 (MORF4L1) is a member of a subgroup of histone acetyltransferases and belongs to the mortality factor on chromosome 4 (MORF4) class of proteins. However, the role of MORF4L1 in cancers is largely unknown. Using reverse transcription-quantitative polymerase chain reaction and published datasets, the present study demonstrated that the expression of MORF4L1 is decreased in several cancers, including nasopharyngeal carcinoma (NPC). Additionally, the methylation rate of the promoter of MORF4L1 was identified to be significantly higher in tumour cells than in normal cells. The ectopic expression of MORF4L1 was also revealed to inhibit cell proliferation, colony formation, migration and invasion in NPC, whereas the knockdown of MORF4L1 promoted cell proliferation, colony formation, migration and invasion. Mechanistically, the present study demonstrated that MORF4L1 functions as a tumour suppressor by increasing p21 and E-cadherin levels. These findings may be useful novel targets for treating patients with NPC.

摘要

死亡因子4样蛋白1(MORF4L1)是组蛋白乙酰转移酶亚组的成员,属于4号染色体上的死亡因子(MORF4)类蛋白质。然而,MORF4L1在癌症中的作用在很大程度上尚不清楚。本研究通过逆转录定量聚合酶链反应和已发表的数据集表明,包括鼻咽癌(NPC)在内的几种癌症中MORF4L1的表达均降低。此外,还发现MORF4L1启动子的甲基化率在肿瘤细胞中显著高于正常细胞。异位表达MORF4L1还可抑制NPC细胞的增殖、集落形成、迁移和侵袭,而敲低MORF4L1则促进细胞增殖、集落形成、迁移和侵袭。从机制上讲,本研究表明MORF4L1通过增加p21和E-钙黏蛋白水平发挥肿瘤抑制作用。这些发现可能是治疗NPC患者有用的新靶点。

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