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DNA replication stress and mitotic catastrophe mediate sotorasib addiction in KRAS G12C -mutant cancer.

Li-Wen ChiouChien-Hui ChanYu-Ling JhuangChing-Yao YangYung-Ming Jeng
Published in: Journal of biomedical science (2023)
We elucidated the mechanisms underlying the sotorasib addiction of cancer cells. Sotorasib addiction appears to be mediated through MAPK pathway hyperactivity, DNA damage, replication stress, and mitotic catastrophe. Moreover, we devised a therapeutic strategy involving a type I BRAF inhibitor to strengthen the effects of sotorasib addiction; this strategy may provide clinical benefit for patients with cancer.
Keyphrases
  • dna damage
  • wild type
  • oxidative stress
  • cell cycle
  • signaling pathway
  • papillary thyroid
  • squamous cell carcinoma
  • cell proliferation