Babraham Institute research uncovers key role of PTPRK in tumor suppression and tissue repair
Researchers at the Babraham Institute have unveiled new insights into the protein PTPRK, which is implicated in various cancers and coeliac disease. Published in the “Journal of Cell Science”, the study highlights PTPRK’s essential role in tumor suppression and tissue repair processes.
Dr. Katie Young, the study’s lead author, explained, “We aimed to investigate PTPRK’s role in the colon, connecting observations in the field back to complex signaling mechanisms.”
The research reveals that the absence of PTPRK in colorectal cancer cells disrupts wound healing and cellular polarization. Animal studies further demonstrate that mice deficient in PTPRK are more prone to colitis and develop larger, more invasive tumors in colorectal cancer models.
Significantly, the study shows that PTPRK’s tumor suppression function operates independently of its phosphatase activity. Gene expression analysis indicates PTPRK’s impact on epithelial cell identity and plasticity, suggesting it is crucial for regulating tissue repair processes. Additionally, PTPRK appears to suppress tumor development by modulating epidermal growth factor receptor (EGFR) signaling.
Dr. Hayley Sharpe, group leader in the Signalling Research Programme at the Institute, commented, “Our goal was to integrate various observations and start addressing the gaps in our understanding of PTPRK. While it was previously thought that PTPs act as tumor suppressors by countering kinase activity through dephosphorylation, PTPRK’s non-catalytic role in signaling presents an intriguing new aspect that requires further investigation to fully comprehend its tumor suppression mechanisms.”
