Recently, numerous studies have reported the interaction between senescence and oxidative stress in cancer. However, there is a lack of a comprehensive understanding of the precise mechanisms involved. Therefore, our review aims to summarize the current findings and elucidate by presenting specific mechanisms that encompass functional pathways, target genes, and related aspects. Pubmed and Web of Science databases were retrieved to search studies about the interaction between senescence and oxidative stress in cancer. Relevant publications in the reference list of enrolled studies were also checked. In carcinogenesis, oxidative stress-induced cellular senescence acts as a barrier against the transformation of stimulated cells into cancer cells. However, the senescence-associated secretory phenotype (SASP) is positively linked to tumorigenesis. In the cancer progression stage, targeting specific genes or pathways that promote oxidative stress-induced cellular senescence can suppress cancer progression. In terms of treatment, many current clinical therapies combine with novel drugs to overcome resistance and reduce side effects by attenuating oxidative stress-induced senescence. Notably, emerging drugs control cancer development by enhancing oxidative stress-induced senescence. These studies highlight the complacted effects of the interplay between oxidative stress and senescence at different cancer stages and among distinct cell populations. Future research should focus on characterizing the roles of distinct senescent cell types in various tumor stages and identifying the specific components of SASP. We've summarized the mechanisms of senescence and oxidative stress in cancer and provided illustrative figures to guide future research in this area.

中文翻译：

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氧化应激与癌症衰老之间的相互作用：机制、治疗意义和未来前景


最近，大量研究报道了癌症中衰老和氧化应激之间的相互作用。然而，人们对所涉及的精确机制缺乏全面的了解。因此，我们的综述旨在总结当前的发现，并通过提出涵盖功能途径、靶基因和相关方面的具体机制来阐明。检索 Pubmed 和 Web of Science 数据库来检索有关癌症衰老和氧化应激之间相互作用的研究。还检查了纳入研究的参考文献列表中的相关出版物。在致癌过程中，氧化应激诱导的细胞衰老充当了阻止受刺激细胞转化为癌细胞的屏障。然而，衰老相关分泌表型（SASP）与肿瘤发生呈正相关。在癌症进展阶段，针对促进氧化应激诱导的细胞衰老的特定基因或途径可以抑制癌症进展。在治疗方面，目前许多临床疗法与新药相结合，通过减轻氧化应激引起的衰老来克服耐药性并减少副作用。值得注意的是，新兴药物通过增强氧化应激诱导的衰老来控制癌症的发展。这些研究强调了不同癌症阶段和不同细胞群之间氧化应激和衰老之间相互作用的复杂影响。未来的研究应侧重于表征不同衰老细胞类型在不同肿瘤阶段中的作用，并确定 SASP 的具体成分。我们总结了癌症中衰老和氧化应激的机制，并提供了说明性的数据来​​指导该领域的未来研究。