放射治疗是现代癌症治疗的基石。治疗方法是将局部放射线沉积到肿瘤上，以抑制细胞生长、增殖和转移，并促进癌细胞死亡。此外，辐射还会影响肿瘤微环境（TME）中的非肿瘤细胞。肿瘤细胞的放射抗性是治疗失败的最常见原因，允许癌细胞存活并随后肿瘤生长。分子放射抗性包括癌细胞固有的遗传和表观遗传特征，或暴露于辐射后获得的特征。此外，癌症干细胞（CSC）和非肿瘤细胞作为基质细胞和免疫细胞进入 TME，在促进和维持放射抗性肿瘤表型方面发挥着作用。抗辐射的不同调节分子和途径包括 DNA 修复、生存信号传导和细胞死亡途径。表观遗传机制是放疗后发生的最相关事件之一，用于调节差异辐射反应中关键基因和蛋白质的表达和功能。本文回顾了与癌症放疗生物反应相关的主要分子机制和信号通路的最新数据；强调 DNA 甲基化、组蛋白标记、染色质重塑和 m6A RNA 甲基化对基因表达和与放射治疗反应相关的信号通路激活所施加的表观遗传控制。版权所有 © 2024。由 Elsevier Inc. 出版。

Radiation therapy is a cornerstone of modern cancer treatment. Treatment is based on depositing focal radiation to the tumor to inhibit cell growth, proliferation and metastasis, and to promote the death of cancer cells. In addition, radiation also affects non-tumor cells in the tumor microenvironmental (TME). Radiation resistance of the tumor cells is the most common cause of treatment failure, allowing survival of cancer cell and subsequent tumor growing. Molecular radioresistance comprises genetic and epigenetic characteristics inherent in cancer cells, or characteristics acquired after exposure to radiation. Furthermore, cancer stem cells (CSCs) and non-tumor cells into the TME as stromal and immune cells have a role in promoting and maintaining radioresistant tumor phenotypes. Different regulatory molecules and pathways distinctive of radiation resistance include DNA repair, survival signaling and cell death pathways. Epigenetic mechanisms are one of the most relevant events that occur after radiotherapy to regulate the expression and function of key genes and proteins in the differential radiation-response. This article reviews recent data on the main molecular mechanisms and signaling pathways related to the biological response to radiotherapy in cancer; highlighting the epigenetic control exerted by DNA methylation, histone marks, chromatin remodeling and m6A RNA methylation on gene expression and activation of signaling pathways related to radiation therapy response.Copyright © 2024. Published by Elsevier Inc.