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Published on: June 17, 2014
TRIM29 prevents hepatocellular carcinoma progression by inhibiting Wnt/β-catenin signaling pathway
Mingxing Xu1, Jingxiong Hu1, Boxuan Zhou1
1Department of Hepatobiliary Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Abstract:
TRIM29 plays an important role in many neoplasms. In this study, we aimed to elucidate its role in hepatocellular carcinoma (HCC) and explore the corresponding potential mechanism. The expression level of TRIM29 in HCC samples and hepatoma cell lines was detected. We found that TRIM29 was down-regulated in clinical HCC samples and cultured hepatoma cell lines by western blot analysis and quantitative polymerase chain reaction. In addition, we demonstrated that higher TRIM29 expression was associated with higher differentiation grade of HCC. To explore the effect of TRIM29 on hepatoma cells and its possible mechanisms, TRIM29-knockdown and overexpression cell models were constructed. The results showed that the depletion of TRIM29 promoted liver cancer cell proliferation, clone formation, migration and invasion in vitro probably through the Wnt/β-catenin signaling pathway. This study revealed the inhibitory roles of TRIM29 in HCC and the possible mechanisms.
Insights
Tripartite motif-containing protein 29 (TRIM29) acts as a tumor suppressor in liver cancer. Lower TRIM29 expression correlates with poor hepatocellular carcinoma (HCC) differentiation and promotes cancer progression via the Wnt/β-catenin pathway.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Tripartite motif-containing protein 29 (TRIM29) is implicated in various cancers.
- Its specific role and mechanism in hepatocellular carcinoma (HCC) require further elucidation.
Purpose of the Study:
- To investigate the expression and function of TRIM29 in HCC.
- To explore the underlying molecular mechanisms of TRIM29's action in liver cancer.
Main Methods:
- Western blot and quantitative polymerase chain reaction (qPCR) to detect TRIM29 expression in HCC tissues and cell lines.
- Construction of TRIM29-knockdown and overexpression HCC cell models.
- In vitro assays to assess cell proliferation, clone formation, migration, and invasion.
Main Results:
- TRIM29 expression was significantly down-regulated in HCC samples and cell lines.
- Reduced TRIM29 levels correlated with lower HCC differentiation.
- TRIM29 depletion enhanced HCC cell proliferation, colony formation, migration, and invasion.
- These effects were associated with the Wnt/β-catenin signaling pathway.
Conclusions:
- TRIM29 functions as a tumor suppressor in HCC.
- Down-regulation of TRIM29 promotes HCC progression, potentially through the Wnt/β-catenin pathway.
- TRIM29 may serve as a potential therapeutic target for HCC.
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