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Published on: October 30, 2013
METTL13 is downregulated in bladder carcinoma and suppresses cell proliferation, migration and invasion
Zhe Zhang1, Guojun Zhang2, Chuize Kong1
1Department of Urology, the First Hospital of China Medical University, Shenyang, 110001, China.
Abstract:
The incidence of bladder cancer has increased in the last few decades, thus novel markers for early diagnosis and more efficacious treatment are urgently needed. It found that METTTL13 protein is aberrant expression in variety of human cancers and METTL13 was involved in oncogenic pathways. However, the role of METTL13 has been unexplored in bladder cancer to date. Here, expression of METTL13 was lower in bladder cancer tissue samples and cancer cell lines than in normal bladder tissue and cell lines. METTL13 was downregulated in the late stages of the disease and was maintained at low level throughout the tumor progression process based on tumor node metastasis (TNM) staging. Further research suggested that METTL13 negatively regulates cell proliferation in bladder cancer and reinstates G1/S checkpoint via the coordinated downregulation of CDK6, CDK4 and CCND1, decreased phosphorylation of Rb and subsequent delayed cell cycle progression. Moreover, METTL13-dependent inhibition of bladder cancer cell migration and invasion is mediated by downregulation of FAK (Focal adhesion kinase) phosphorylation, AKT (v-akt murine thymoma viral oncogene) phosphorylation, β-catenin expression and MMP-9 expression. These integrated efforts have identified METTL13 as a tumor suppressor and might provide promising approaches for bladder cancer treatment and prevention.
Insights
METTL13 protein acts as a tumor suppressor in bladder cancer, with its reduced expression linked to advanced disease stages. Restoring METTL13 may offer new therapeutic strategies for bladder cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Bladder cancer incidence is rising, necessitating new diagnostic markers and treatments.
- METTL13 protein shows aberrant expression in various cancers and is implicated in oncogenic pathways.
- The specific role of METTL13 in bladder cancer remains largely uninvestigated.
Purpose of the Study:
- To investigate the expression and function of METTL13 in bladder cancer.
- To determine METTL13's potential as a tumor suppressor in bladder cancer.
- To explore METTL13's impact on bladder cancer cell proliferation, migration, and invasion.
Main Methods:
- Quantitative analysis of METTL13 expression in bladder cancer tissues and cell lines compared to normal controls.
- Correlation analysis of METTL13 expression with tumor stage (TNM staging).
- In vitro studies assessing the effects of METTL13 on cell cycle regulation (CDK6, CDK4, CCND1, Rb phosphorylation) and cell motility (FAK, AKT, β-catenin, MMP-9 phosphorylation).
Main Results:
- METTL13 expression was significantly lower in bladder cancer tissues and cell lines than in normal counterparts.
- METTL13 downregulation correlated with advanced tumor stages and progression.
- METTL13 suppressed bladder cancer cell proliferation by reinstating the G1/S checkpoint and inhibited migration and invasion by downregulating key signaling molecules.
Conclusions:
- METTL13 functions as a tumor suppressor in bladder cancer.
- Reduced METTL13 expression is associated with disease progression.
- METTL13 represents a potential therapeutic target for bladder cancer treatment and prevention.
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