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Updated: May 1, 2026

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
Published on: August 5, 2022
CMTM5 exhibits tumor suppressor activity through promoter methylation in oral squamous cell carcinoma
Heyu Zhang1, Xu Nan2, Xuefen Li1
1Central Laboratory, Peking University School of Stomatology, Beijing, China.
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.
Insights
CKLF-like MARVEL transmembrane domain-containing member 5 (CMTM5) acts as a tumor suppressor in oral squamous cell carcinoma (OSCC). Its down-regulation, due to promoter methylation, inhibits OSCC progression and tumor formation.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Oral squamous cell carcinoma (OSCC) is a prevalent head and neck malignancy.
- CKLF-like MARVEL transmembrane domain-containing member 5 (CMTM5) is recognized as a potential tumor suppressor in various cancers.
Purpose of the Study:
- To investigate the expression and functional role of CMTM5 in oral squamous cell carcinoma.
- To determine the mechanism of CMTM5 down-regulation in OSCC.
Main Methods:
- Analysis of CMTM5 expression in OSCC cell lines and patient tumor samples.
- Investigation of promoter methylation as a cause for CMTM5 down-regulation.
- Assessment of CMTM5 restoration using 5-aza-2'-deoxycytidine.
- Evaluation of CMTM5-v1 ectopic expression effects on OSCC cell proliferation, migration, and apoptosis in vitro.
- In vivo tumor formation assays.
Main Results:
- CMTM5 expression was significantly down-regulated in OSCC cell lines and tumor tissues.
- Promoter methylation was identified as the mechanism for CMTM5 down-regulation.
- Demethylating agent treatment restored CMTM5 expression.
- Ectopic CMTM5-v1 expression suppressed OSCC cell proliferation and migration, and induced apoptosis.
- CMTM5-v1 inhibited tumor formation in vivo.
Conclusions:
- CMTM5 functions as a tumor suppressor in oral squamous cell carcinoma.
- Promoter methylation-induced down-regulation of CMTM5 contributes to OSCC development.
- CMTM5 represents a potential therapeutic target for oral squamous cell carcinoma.
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