| Autor: |
Técher, Hervé, Kemiha, Samira, Aobuli, Xieraili, Kolinjivadi, Arun Mouli |
| Předmět: |
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| Zdroj: |
Cancers; Dec2024, Vol. 16 Issue 23, p3993, 19p |
| Abstrakt: |
Simple Summary: Oncogenes are proteins promoting cancer formation. Cancers caused by mutations in the RAS oncogene have been a major focus of cancer research for decades. Despite better understanding of how the RAS oncogene works, finding an effective way to treat RAS-driven cancers remains a challenge. This review explores how RAS affects DNA replication and genome stability. It also describes how RAS can lead to inflammatory responses and senescence. Finally, we discuss how these molecular insights have led to potential new lines of treatments to target RAS-mutated cancers. Rat Sarcoma (RAS)-driven cancers have been one of the main foci in the field of cancer science for over four decades. Despite significant improvement in understanding the biology of RAS oncogene, the method to target RAS-mutated cancers is still unclear. In recent years, the role for RAS beyond its hyperproliferation has been extensively documented. In this review, we systematically address and dwell on the details of the mechanisms of RAS oncogene-mediated alteration in the DNA replication and DNA damage response (DDR) pathways, focusing on lung cancers. We further extend this molecular connection towards cytosolic DNA accumulation, innate immune activation and senescence in RAS-addicted cancers. At the end, we briefly speculate on the potential strategies for targeting RAS mutated lung cancers, considering various approaches targeting DNA replication, DNA repair and the cGAS-STING pro-inflammatory pathway. These new lines of therapy, especially when used in combinations, may enhance treatment efficacy and overcome the challenges associated with these mutations. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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