Huang Qi, Jing Yuan, Xiong Lihua, Li Lei, Feng Jingjuan, Cheng Jian
Department of Anorectal Surgery, The People's Hospital of Leshan, Leshan, 614000, China.
Department of Medical Records, The People's Hospital of Leshan, Leshan, 614000, China.
J Transl Med. 2025 Jun 9;23(1):635. doi: 10.1186/s12967-025-06640-x.
Colorectal cancer (CRC) is a multifaceted disease influenced by genetic mutations and environmental factors, especially oxidative stress. Driver mutations are pivotal in CRC initiation and progression and alter key signaling pathways involved in cell proliferation, apoptosis, and genomic stability. Concurrently, oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, plays a crucial role in CRC development by promoting DNA damage, lipid peroxidation, and redox signaling dysregulation. The molecular mechanisms linking driver mutations and oxidative stress pathways underscore their collective or antagonistic impact on CRC heterogeneity, therapeutic responses, and clinical outcomes. Insights into mutation-specific vulnerabilities and redox modulation offer promising avenues for targeted therapies and personalized medicine approaches in CRC treatment. Here, we discuss the intricate interplay between driver mutations and oxidative stress, highlight emerging trends, and propose future research directions to advance our understanding of CRC pathogenesis and optimize therapeutic interventions.
结直肠癌（CRC）是一种受基因突变和环境因素影响的多方面疾病，尤其是氧化应激。驱动突变在CRC的发生和发展中起关键作用，并改变参与细胞增殖、凋亡和基因组稳定性的关键信号通路。同时，以活性氧（ROS）产生与抗氧化防御之间失衡为特征的氧化应激，通过促进DNA损伤、脂质过氧化和氧化还原信号失调，在CRC发展中起关键作用。连接驱动突变和氧化应激途径的分子机制强调了它们对CRC异质性、治疗反应和临床结果的共同或拮抗影响。对突变特异性脆弱性和氧化还原调节的深入了解为CRC治疗中的靶向治疗和个性化医疗方法提供了有前景的途径。在此，我们讨论驱动突变与氧化应激之间的复杂相互作用，突出新出现的趋势，并提出未来研究方向，以增进我们对CRC发病机制的理解并优化治疗干预措施。
