Autophagy: cancer's friend or foe?
Autophagy: cancer's friend or foe?
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DOI：
10.1016/b978-0-12-407173-5.00003-0
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发表时间：
2013
影响因子：
--
通讯作者：
Fisher, Paul B.
中科院分区：
文献类型：
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作者：
Bhutia, Sujit K.;Mukhopadhyay, Subhadip;Sinha, Niharika;Das, Durgesh Nandini;Panda, Prashanta Kumar;Patra, Samir K.;Maiti, Tapas K.;Mandal, Mahitosh;Dent, Paul;Wang, Xiang-Yang;Das, Swadesh K.;Sarkar, Devanand;Fisher, Paul B.
自噬在肿瘤形成和进展中的功能相关性仍存在争议。自噬可以在癌症发生过程中促进肿瘤抑制，并在进展过程中保护肿瘤。自噬相关的细胞死亡可能充当肿瘤抑制因子，一些与自噬相关的基因在癌症中被删除。在小鼠肿瘤模型中，自噬的丧失会导致基因组不稳定和炎症坏死。相反，自噬增强了遭受代谢应激的肿瘤细胞的存活，并可能通过增强肿瘤细胞在环境应激下的存活来促进转移。揭示自噬的复杂分子调控和多种不同作用对于指导合理和新型癌症疗法的开发至关重要。
The functional relevance of autophagy in tumor formation and progression remains controversial. Autophagy can promote tumor suppression during cancer initiation and protect tumors during progression. Autophagy-associated cell death may act as a tumor suppressor, with several autophagy-related genes deleted in cancers. Loss of autophagy induces genomic instability and necrosis with inflammation in mouse tumor models. Conversely, autophagy enhances survival of tumor cells subjected to metabolic stress and may promote metastasis by enhancing tumor cell survival under environmental stress. Unraveling the complex molecular regulation and multiple diverse roles of autophagy is pivotal in guiding development of rational and novel cancer therapies.