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CMTM5 exhibits tumor suppressor activity through promoter methylation in oral squamous cell carcinoma.
- Source :
-
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2014 May 02; Vol. 447 (2), pp. 304-10. Date of Electronic Publication: 2014 Apr 08. - Publication Year :
- 2014
-
Abstract
- Oral squamous cell carcinoma (OSCC) is one of the most common types of malignancies in the head and neck region. CKLF-like MARVEL transmembrane domain-containing member 5 (CMTM5) has been recently implicated as a tumor suppressor gene in several cancer types. Herein, we examined the expression and function of CMTM5 in oral squamous cell carcinoma. CMTM5 was down-regulated in oral squamous cell lines and tumor samples from patients with promoter methylation. Treatment with the demethylating agent 5-aza-2'-deoxycytidine restored CMTM5 expression. In the OSCC cell lines CAL27 and GNM, the ectopic expression of CMTM5-v1 strongly inhibited cell proliferation and migration and induced apoptosis. In addition, CMTM5-v1 inhibited tumor formation in vivo. Therefore, CMTM5 might act as a putative tumor suppressor gene through promoter methylation in oral squamous cell carcinoma.<br /> (Copyright © 2014 Elsevier Inc. All rights reserved.)
- Subjects :
- Adult
Carcinoma, Squamous Cell pathology
Cell Line, Tumor
Chemokines genetics
Down-Regulation
Female
Gene Expression Regulation, Neoplastic
Humans
MARVEL Domain-Containing Proteins genetics
Male
Middle Aged
Mouth Neoplasms pathology
Promoter Regions, Genetic
Tumor Suppressor Proteins genetics
Young Adult
Carcinoma, Squamous Cell genetics
Chemokines metabolism
DNA Methylation
MARVEL Domain-Containing Proteins metabolism
Mouth Neoplasms genetics
Tumor Suppressor Proteins metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1090-2104
- Volume :
- 447
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Biochemical and biophysical research communications
- Publication Type :
- Academic Journal
- Accession number :
- 24721428
- Full Text :
- https://doi.org/10.1016/j.bbrc.2014.03.158