Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma
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Updated: Dec 16, 2025

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Published on: October 27, 2020
Shidong Zhang1, Run Tian1, Chunhua Bei1
1Department of Epidemiology and Health Statistics, School of Public Health, Guilin Medical University, Guilin 541199, Guangxi, People's Republic of China.
Background:
Our recent study identified that human chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family member 2 (CMTM2) was deregulated in hepatocellular carcinoma (HCC) tissues and posed as a potential tumor suppressor. However, the mechanism of CMTM2 in HCC occurrence and development has not been well elaborated.
Materials And Methods:
The expression of CMTM2 was knocked-down by RNA interruption in Huh-7 and SMMC7721 cells. Cell proliferation ability was detected by CCK8 test and colony formation assay. The cell invasion and migration were measured by wound healing and Transwell assay.
Results:
We found that the cell proliferation was significantly increased by interruption of CMTM2 expression, both in Huh-7 and SMMC7721 cells. Moreover, down-regulated CMTM2 could promote the invasion and migration ability of HCC cells through inducing the epithelial-mesenchymal transition (EMT) process. We further discovered that both the expression of CMTM2 and the EMT-associated marker E-cadherin were decreased in the same thirty cases of HCC tissues compared with the corresponding adjacent non-tumor tissues. Pearson correlation test showed that there was a significantly positive correlation between CMTM2 and E-cadherin in HCC tissues (P<0.05).
Conclusion:
Based on the results of cell model and HCC tissues, our study suggests that down-regulated CMTM2 promotes HCC metastasis through inducing the EMT process.
Insights
Down-regulated chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family member 2 (CMTM2) promotes hepatocellular carcinoma (HCC) metastasis. Reduced CMTM2 expression enhances HCC cell proliferation, invasion, and migration by inducing epithelial-mesenchymal transition (EMT).
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family member 2 (CMTM2) is deregulated in hepatocellular carcinoma (HCC).
- CMTM2 functions as a potential tumor suppressor in HCC.
- The precise mechanism of CMTM2 in HCC progression remains unclear.
Purpose of the Study:
- To elucidate the mechanism by which CMTM2 influences HCC occurrence and development.
- To investigate the role of CMTM2 in HCC cell proliferation, invasion, and migration.
- To analyze the correlation between CMTM2 expression and epithelial-mesenchymal transition (EMT) markers in HCC tissues.
Main Methods:
- CMTM2 expression was suppressed using RNA interference in HCC cell lines (Huh-7 and SMMC7721).
- Cell proliferation was assessed via CCK-8 assay and colony formation assays.
- Cell invasion and migration were evaluated using wound healing and Transwell assays.
Main Results:
- CMTM2 knockdown significantly increased HCC cell proliferation, invasion, and migration.
- Down-regulated CMTM2 induced the epithelial-mesenchymal transition (EMT) process in HCC cells.
- Both CMTM2 and E-cadherin expression were decreased in HCC tissues compared to adjacent non-tumor tissues, with a positive correlation between them.
Conclusions:
- Reduced CMTM2 expression promotes HCC metastasis by inducing EMT.
- CMTM2 acts as a tumor suppressor in HCC by inhibiting EMT and metastasis.
- Findings highlight CMTM2 as a potential therapeutic target for HCC treatment.
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