What's Happening?
Researchers at Singapore's A*STAR Institute of Molecular and Cell Biology have identified a mechanism that allows certain lung cancer cells to resist treatment. The study, published in Science Advances,
reveals that mutations in the EGFR gene lead to the production of stable mutant proteins that evade degradation. The team discovered that cancer cells use ATP to activate the P2Y2 receptor, which partners with integrin β1 to form a protective barrier around these proteins. This barrier prevents the proteins from being broken down, allowing them to continue driving cancer growth. The findings were confirmed in human tissue samples, showing elevated levels of P2Y2 and integrin β1 in tumors.
Why It's Important?
This discovery is crucial as it uncovers a new target for overcoming drug resistance in lung cancer, a major challenge in cancer treatment. By understanding the 'bodyguard' system that protects mutant proteins, researchers can develop strategies to disrupt this mechanism, potentially improving the effectiveness of existing treatments. The study also highlights the potential of using natural compounds like kaempferol to target this system, offering a new approach to combat drug-resistant lung cancer. This could lead to more effective therapies and improved survival rates for patients with EGFR-mutant lung cancer.
What's Next?
The researchers plan to further explore the P2Y2-integrin axis as a therapeutic target. Future studies will focus on developing drugs that can effectively disrupt this protective mechanism in cancer cells. Additionally, clinical trials may be conducted to test the efficacy of kaempferol and other compounds in human patients. If successful, these efforts could lead to new combination therapies that enhance the effectiveness of current treatments and prevent the development of drug resistance.
