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Published on: October 30, 2013
CMTM8 inhibits the carcinogenesis and progression of bladder cancer
Abstract:
Bladder cancer is the most common tumor of the urinary tract. The incidence of bladder cancer has increased in the last few decades, thus novel molecular markers for early diagnosis and more efficacious treatment are urgently needed. Chemokine‑like factor (CKLF)‑like MARVEL transmembrane domain containing 8 (CMTM8) is downregulated in several types of cancers and is associated with tumor progression. However, CMTM8 expression has been unexplored in bladder cancer to date. Our results revealed that the expression of CMTM8 was negative in 46 of 74 (62.2%) bladder cancer samples via immunohistochemistry assay. CMTM8 downregulation was associated with advancing tumor stage and tumor grade. CMTM8 was successfully overexpressed by lentivirus in EJ and T24 cells, and the CCK‑8 and Transwell assays showed that CMTM8 overexpression decreased cell proliferation, migration and invasion in vitro. In tumor xenografts upregulation of CMTM8 inhibited tumor growth and lymph node metastasis in vivo. In conclusion, overexpression of CMTM8 in bladder cancer results in reduced malignant cell growth, migration and invasion, which could make it a potential therapeutic target in the treatment of bladder cancer.
Insights
Chemokine-like factor transmembrane domain containing 8 (CMTM8) is often lost in bladder cancer. Restoring CMTM8 reduced cancer cell growth, migration, and invasion, suggesting it as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Uro-oncology
Background:
- Bladder cancer incidence is rising, necessitating new diagnostic markers and treatments.
- Chemokine-like factor transmembrane domain containing 8 (CMTM8) is downregulated in various cancers, impacting tumor progression.
- CMTM8's role in bladder cancer remains largely uninvestigated.
Purpose of the Study:
- To investigate CMTM8 expression in bladder cancer.
- To determine the association between CMTM8 expression and clinicopathological features.
- To evaluate the functional role of CMTM8 in bladder cancer progression.
Main Methods:
- Immunohistochemistry was used to assess CMTM8 expression in 74 bladder cancer samples.
- Lentivirus-mediated gene delivery was employed for CMTM8 overexpression in bladder cancer cell lines (EJ and T24).
- Cell Counting Kit-8 (CCK-8) and Transwell assays were performed to assess cell proliferation, migration, and invasion in vitro. Tumor xenograft models were used for in vivo studies.
Main Results:
- CMTM8 expression was found to be negative in 62.2% of bladder cancer samples.
- Downregulation of CMTM8 correlated with advanced tumor stage and higher tumor grade.
- Overexpression of CMTM8 significantly inhibited bladder cancer cell proliferation, migration, and invasion in vitro and suppressed tumor growth and lymph node metastasis in vivo.
Conclusions:
- CMTM8 is frequently downregulated in bladder cancer and its expression is linked to poorer clinicopathological outcomes.
- Upregulation of CMTM8 suppresses malignant behaviors of bladder cancer cells.
- CMTM8 represents a promising molecular target for bladder cancer therapy.
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