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

Hyun Ju Woo | Zendy; Sung Jin Kim | Zendy; KYUNG-JOO SONG | Zendy; Sung Soon Kim | Zendy; CheolHee Yoon | Zendy; ByeongSun Choi | Zendy; Jee Eun Rhee | Zendy

Open Access

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

Author(s) -

Hyun Ju Woo,

Sung Jin Kim,

KYUNG-JOO SONG,

Sung Soon Kim,

CheolHee Yoon,

ByeongSun Choi,

Jee Eun Rhee

Publication year - 2015

Publication title -

international journal of oncology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.405

H-Index - 122

ISSN - 1019-6439

DOI - 10.3892/ijo.2015.2945

Subject(s) - cancer research , biology , oncogene , cell adhesion molecule , epigenetics , tumor suppressor gene , cancer , l1 , cell cycle , cell , cell adhesion , suppressor , carcinogenesis , immunology , gene , genetics

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.

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