CMTM5 exhibits tumor suppressor activity through promoter methylation in oral squamous cell carcinoma

Journal Article · Fri May 02 00:00:00 EDT 2014 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2014.03.158· OSTI ID:22416414

Zhang, Heyu ^[1]; Nan, Xu ^[2]; Li, Xuefen ^[1]; Chen, Yan; Zhang, Jianyun ^[3]; Sun, Lisha ^[1]; Han, Wenlin ^[2]; Li, Tiejun ^[3]

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1. Central Laboratory, Peking University School of Stomatology, Beijing (China)
2. Center for Human Disease Genomics, Department of Immunology, Key Laboratory of Medical Immunology, Ministry of Health, School of Basic Medical Sciences, Peking University, Beijing (China)
3. Department of Oral Pathology, Peking University School of Stomatology, Beijing (China)

Highlights: • Down-regulation of CMTM5 expression in OSCC tissues was found. • The promoter methylation status of CMTM5 was measured. • CMTM5-v1 inhibited cell proliferation and migration and induced apoptosis. • CMTM5 might act as a putative tumor suppressor gene in OSCC. - 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.

• OSTI ID: 22416414
• Journal Information: Biochemical and Biophysical Research Communications, Vol. 447, Issue 2; Other Information: Copyright (c) 2014 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ANIMAL TISSUES
APOPTOSIS
CARCINOMAS
CELL PROLIFERATION
DEOXYCYTIDINE
GENES
IN VIVO
METHYLATION
MIGRATION
NECK
PATIENTS
PROMOTERS