Capn4 promotes colorectal cancer cell proliferation by increasing MAPK7 through activation of the Wnt/β-Catenin pathway
- Department of Gastrointestinal Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006 (China)
Highlights: • Capn4 is upregulated in colorectal cancer (CRC) tissues and is closely correlated with clinical outcomes. • Capn4 knockdown significantly suppresses CRC cell growth in vitro and in vivo. • MAPK7 acts as the downstream component of Capn4 and contributes the effects of Capn4 in CRC cells. • Capn4 positively regulates MAPK7 expression through the Wnt/β-Catenin pathway in CRC cells. Increasing evidence has suggested that Capn4 is upregulated and functions as a potential tumor promoter in several human cancer types. However, the potential biological roles and regulatory mechanisms of Capn4 in colorectal cancer (CRC) remains unclear. Here, we found that Capn4 expression was elevated in CRC tissues than adjacent noncancerous tissues. Additionally, we also found that overexpression of Capn4 is significantly correlated with tumor progression and poor survival in CRC patients. Furthermore, our experimental data revealed that increased expression of Capn4 was observed in CRC cell lines and ectopic expression of Capn4 significantly enhanced in vitro cell proliferation, whereas knockdown of Capn4 suppressed CRC cells growth in vitro and in vivo. Moreover, our results indicate that Capn4 promotes cell proliferation by increasing MAPK7 expression, which has been reported to control the proliferation of many cancers. Mechanistically, Capn4 upregulates MAPK7 expression through activation of the Wnt/β-Catenin pathway in CRC cells. Therefore, we identified a tumorigenic role of Capn4 in CRC and suggested a potential therapeutic target for CRC patients.
- OSTI ID:
- 23082466
- Journal Information:
- Experimental Cell Research, Journal Name: Experimental Cell Research Journal Issue: 2 Vol. 363; ISSN 0014-4827; ISSN ECREAL
- Country of Publication:
- United States
- Language:
- English
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