Prkci promotes colorectal cancer metastasis by phosphorylating and stabilizing Tgfbr1 to activate TGF-β signaling.
Article
Li, Peng, Liu, Guangshi, Zhang, Wenbin et al. (2025). Prkci promotes colorectal cancer metastasis by phosphorylating and stabilizing Tgfbr1 to activate TGF-β signaling.
. Cell Communication and Signaling, 23(1), 230. 10.1186/s12964-025-02236-6
Li, Peng, Liu, Guangshi, Zhang, Wenbin et al. (2025). Prkci promotes colorectal cancer metastasis by phosphorylating and stabilizing Tgfbr1 to activate TGF-β signaling.
. Cell Communication and Signaling, 23(1), 230. 10.1186/s12964-025-02236-6
Colorectal cancer is one of the most common malignancies worldwide, with metastasis being the leading cause of cancer-related mortality. However, the molecular mechanisms driving CRC metastasis remain poorly understood. In this study, we identified Prkci as a critical oncogenic driver in CRC metastasis. Prkci was significantly upregulated in metastatic CRC tissues. Mechanistically, Prkci phosphorylated and stabilized Tgfbr1, a key receptor in the Transforming Growth Factor Beta signaling pathway, preventing its proteasomal degradation and amplifying downstream signaling cascades. This stabilization promoted epithelial-to-mesenchymal transition, enhancing migratory and invasive capacities of CRC cells. In vivo, Prkci knockout significantly reduced liver and lung metastases and prolonged survival in mouse models, highlighting its therapeutic potential. These findings establish Prkci as a promising therapeutic target for suppressing CRC metastasis and improving outcomes for metastatic CRC patients.
