PTPRK, or Protein Tyrosine Phosphatase Receptor Type K, is a protein known for its role in various cellular processes. It’s been linked to several types of cancer and coeliac disease. The new study sheds light on its crucial role in maintaining cell health and preventing cancerous growths.
Researchers at the Babraham Institute have made a breakthrough in understanding PTPRK, a protein linked to cancer and coeliac disease. Their findings, published in the Journal of Cell Science, offer new insights into how PTPRK functions in tumour suppression and tissue repair.
The Study’s Key Findings
The research team, led by Dr. Katie Young, discovered that PTPRK plays a vital role in the colon. When PTPRK was removed from colorectal cancer cells, the cells struggled with wound healing and maintaining their structure. This was observed in mice as well, where the absence of PTPRK led to more severe colitis and larger, more invasive tumours.
Beyond Phosphatase Activity
One of the most ground-breaking discoveries is that PTPRK’s ability to suppress tumours doesn’t rely on its phosphatase activity. This challenges the traditional view of how Protein Tyrosine Phosphatases (PTPs) function in cancer suppression. Instead, PTPRK impacts gene expression related to epithelial cell identity and tissue repair.
PTPRK and EGFR Signalling
The study also highlights how PTPRK regulates Epidermal Growth Factor Receptor (EGFR) signalling. EGFR is a pathway often implicated in cancer development. By influencing this pathway, PTPRK further solidifies its role as a tumour suppressor.
Implications for Cancer Treatment
The discovery that PTPRK can suppress tumours without relying on its phosphatase activity opens new avenues for cancer treatment. Understanding these mechanisms could lead to more effective therapies targeting PTPRK and similar proteins.
The Role in Coeliac Disease
While the study primarily focuses on cancer, the findings also have implications for coeliac disease. PTPRK’s role in tissue repair and cell health is crucial for understanding how to manage and potentially treat coeliac disease.
Dr. Katie Young emphasized the importance of these findings, stating, “We aimed to connect our observations in the colon to broader signalling mechanisms.” Dr. Hayley Sharpe, another key researcher, added, “The non-catalytic role of PTPRK in signalling is really intriguing to us and how it achieves this is an important next question to fully understand its role in tumour suppression.”
The team plans to further explore how PTPRK achieves its non-catalytic role in signalling. This research could lead to significant advancements in both cancer and coeliac disease treatments.
This study offers ground-breaking insights into the role of PTPRK in cancer and coeliac disease. By understanding how PTPRK functions, researchers hope to develop more effective treatments for these conditions. The Babraham Institute’s research marks a significant step forward in the fight against cancer and the quest for better management of coeliac disease.