Exploiting tumor cell senescence in anticancer therapy.
Exploiting tumor cell senescence in anticancer therapy.
复制标题
DOI：
10.5483/bmbrep.2014.47.2.005
复制
发表时间：
2014-02
期刊：
影响因子：
3.8
通讯作者：
Lee JS
中科院分区：
文献类型：
--
作者：
Lee M;Lee JS
细胞衰老是一种细胞周期不可逆停滞的生理过程，参与了衰老的各种生理和病理过程。而复制性衰老与重复细胞分裂后的端粒磨损有关，应激诱导的早衰发生在异常致癌信号，氧化应激和DNA损伤，这是独立的端粒功能障碍。最近的证据表明，细胞衰老为肿瘤发生提供了屏障，并且是癌症治疗结果的决定因素。然而，衰老相关的分泌表型，这有助于衰老癌细胞的多个方面，可能会影响相邻细胞的抑癌和促癌机制。常规治疗，如化疗和放疗，优先诱导早衰，而不是在适当的细胞凋亡的情况下。此外，治疗诱导的过早衰老可以通过替代信号通路补偿对细胞凋亡的抵抗。因此，我们相信，深入了解癌细胞衰老可以促进开发新的治疗策略，以提高抗癌治疗的疗效。本文综述了细胞衰老的分子机制、功能及其在抗肿瘤治疗中的临床应用。[BMB报告2014; 47（2）：51-59]
Cellular senescence is a physiological process of irreversible cell-cycle arrest that contributes to various physiological and pathological processes of aging. Whereas replicative senescence is associated with telomere attrition after repeated cell division, stress-induced premature senescence occurs in response to aberrant oncogenic signaling, oxidative stress, and DNA damage which is independent of telomere dysfunction. Recent evidence indicates that cellular senescence provides a barrier to tumorigenesis and is a determinant of the outcome of cancer treatment. However, the senescence-associated secretory phenotype, which contributes to multiple facets of senescent cancer cells, may influence both cancer-inhibitory and cancer-promoting mechanisms of neighboring cells. Conventional treatments, such as chemo- and radiotherapies, preferentially induce premature senescence instead of apoptosis in the appropriate cellular context. In addition, treatment-induced premature senescence could compensate for resistance to apoptosis via alternative signaling pathways. Therefore, we believe that an intensive effort to understand cancer cell senescence could facilitate the development of novel therapeutic strategies for improving the efficacy of anticancer therapies. This review summarizes the current understanding of molecular mechanisms, functions, and clinical applications of cellular senescence for anticancer therapy. [BMB Reports 2014; 47(2): 51-59]
登录
查看更多内容
影响因子：
11.2
作者：
Bavik, C;Coleman, I;Nelson, PS
通讯作者：
Nelson, PS
DOI：
10.1146/annurev-pathol-121808-102144
发表时间：
2010
期刊：
Annual review of pathology
影响因子：
--
作者：
Coppé JP;Desprez PY;Krtolica A;Campisi J
通讯作者：
Campisi J
影响因子：
5
作者：
Deng, Yibin;Chang, Sandy
通讯作者：
Chang, Sandy
影响因子：
7.5
作者：
Chandler, Hollie;Peters, Gordon
通讯作者：
Peters, Gordon
影响因子：
4.3
作者：
Acosta, Juan C.;O'Loghlen, Ana;Gil, Jesus
通讯作者：
Gil, Jesus