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人乳头瘤病毒转化的宫颈癌细胞中肿瘤抑制细胞粘附分子1的高甲基化

Hypermethylation of the tumor-suppressor cell adhesion molecule 1 in human papillomavirus-transformed cervical carcinoma cells.

作者信息

Woo Hyun Ju, Kim Sung Jin, Song Kyung-Joo, Kim Sung Soon, Yoon Cheol-Hee, Choi Byeong-Sun, Rhee Jee Eun

机构信息

Division of AIDS, Center for Immunology and Pathology, Korea National Institute of Health, Chungbuk, Republic of Korea.

出版信息

Int J Oncol. 2015;46(6):2656-62. doi: 10.3892/ijo.2015.2945. Epub 2015 Apr 1.

Abstract

Epigenetic modification at CpG islands located on the promoter regions of tumor-suppressor genes has been associated with tumor development in many human cancers. Our study showed that the cell adhesion molecule 1 (CADM1) is downregulated in human papillomavirus (HPV)-infected cervical cancer cell lines via its hypermethylation and demethylation using 5-aza-2'-deoxycyticine (5-aza-dC) restored the expression of CADM1 protein. Overexpression of CADM1 inhibited cell proliferation. p53 was involved in the regulation of CADM1. Our results demonstrate that epigenetic alteration of CADM1 was more frequent in HPV-positive cervical cancers and that restoration of CADM1 expression may be a potential strategy for cervical cancer therapy.

摘要

位于肿瘤抑制基因启动子区域的CpG岛的表观遗传修饰与许多人类癌症的肿瘤发生有关。我们的研究表明,细胞粘附分子1(CADM1)在人乳头瘤病毒(HPV)感染的宫颈癌细胞系中通过其高甲基化而下调,并且使用5-氮杂-2'-脱氧胞苷(5-aza-dC)进行去甲基化可恢复CADM1蛋白的表达。CADM1的过表达抑制细胞增殖。p53参与了CADM1的调节。我们的结果表明,CADM1的表观遗传改变在HPV阳性宫颈癌中更为常见,并且恢复CADM1表达可能是宫颈癌治疗的一种潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b37a/4441298/92ab0cc6c95f/IJO-46-06-2656-g00.jpg

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