The role of p53-mediated signaling pathways in nicotine-induced cancer: a systematic review.
Qinhan Jiang, Zhongwei Zhang, Jianming Zhou et al.
✦ AI-curated · Sources linked
In 30 seconds
This systematic review investigates the role of nicotine in modulating p53-mediated signaling pathways in lung, gastric, liver, and cervical cancers. It highlights that nicotine inhibits wild-type p53 activity while enhancing the gain-of-function of mutant p53, particularly p53-RS, promoting cancer progression. The review underscores nicotine's significant role as a tumor promoter, challenging its traditional classification as non-carcinogenic.
Key findings
- In lung cancer, nicotine activates pathways that inhibit p53 and promote proliferation and angiogenesis.
- Nicotine suppresses p53-mediated cell cycle arrest in gastric cancer through specific signaling pathways.
- In liver cancer, nicotine enhances mutant p53 activity and suppresses wild-type p53 expression.
- Cervical cancer progression is driven by nicotine via pathways that involve p53 and cell cycle regulators.
Why it matters
Understanding nicotine's role in cancer biology is crucial for clinicians, as it challenges previous notions of nicotine's safety and highlights its potential as a target for therapeutic intervention in smoking-related cancers.