ArticleCell communication and signaling : CCS2025
Prkci promotes colorectal cancer metastasis by phosphorylating and stabilizing Tgfbr1 to activate TGF-β signaling.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- KRAS-ERK signaling drives metastasis in colorectal cancer via phosphorylation-dependent activation of the ZBTB20-TGFBR2 axis.Journal of experimental & clinical cancer research : CR · 2026Article
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4 authors.
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Abstract
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.
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