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.
Highlights
Cervical cancer is one of the most common malignancies affecting women worldwide, and it is estimated that cervical carcinoma is responsible for 274,000 deaths annually [1]
To explore whether human papillomavirus (HPV) infection is related to cell adhesion molecule 1 (CADM1) expression, we investigated the level of CADM1 in various cervical cancer cells, such as C33A (HPV-negative), HeLa (HPV18-positive), SiHa and CaSki (HPV16-positive) cells
The cell adhesion molecule 1 (CADM1) gene, which is known as TSLC1 or Necl-2, has been generally investigated as a tumor-suppressor gene in various tumors, including prostate, esophageal, nasopharyngeal, non-small cell lung and cervical cancers [16,18,23,24,25]
Summary
Cervical cancer is one of the most common malignancies affecting women worldwide, and it is estimated that cervical carcinoma is responsible for 274,000 deaths annually [1]. Carcinogenesis by hr-HPV relies primarily on the expression of two virally encoded oncoproteins, E6 and E7 [3]. These act synergistically to immortalize and transform the infected cells, partly via their ability to degrade p53 and Rb, respectively [4]. P53 is a tumor-suppressor protein with a sequence-specific DNA-binding domain that plays an important role in transcriptional regulation [5,6]. Previous data related to cervical cancer showed that DAPK1, FHIT, MGMT, CDKN2A, CADM1 and MAL were frequently methylated genes in cervical carcinogenesis [12,15]
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