Cytotoxic autophagy in cancer therapy.
Cytotoxic autophagy in cancer therapy.
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DOI：
10.3390/ijms150610034
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发表时间：
2014-06-05
影响因子：
5.6
通讯作者：
Gewirtz DA
中科院分区：
文献类型：
--
作者：
Sharma K;Le N;Alotaibi M;Gewirtz DA
自噬是细胞自我消化的过程，在这种过程中，细胞降解亚细胞物质以产生能量和代谢前体以延长生存时间，典型的情况是在营养缺乏的情况下。自噬还可能涉及受损或老化的细胞器的降解，以及错误折叠或受损的蛋白质，以消除这些成分，否则这些成分可能对细胞生存有害。因此，自噬通常被认为是一种生存反应。许多化疗药物和放射治疗也促进自噬，这通常被认为是一种细胞保护反应，因为它的抑制经常促进凋亡细胞的死亡。此外，已有研究表明，仅靠常规化疗药物和放射治疗很少引起自噬，从而导致细胞死亡。然而，文献中有多个例子表明，较新的化疗药物、药物组合或与辐射联合使用的药物促进自噬细胞死亡。本文将描述在乳腺肿瘤细胞、肺癌细胞和胶质母细胞瘤中诱导的自噬细胞死亡，表明不能得出应激诱导的自噬必然具有细胞保护功能的结论。
Autophagy is a process of cellular self-digestion, whereby the cell degrades subcellular materials in order to generate energy and metabolic precursors in order to prolong survival, classically under conditions of nutrient deprivation. Autophagy can also involve the degradation of damaged or aged organelles, and misfolded or damaged proteins to eliminate these components that might otherwise be deleterious to cellular survival. Consequently, autophagy has generally been considered a prosurvival response. Many, if not most chemotherapeutic drugs and radiation also promote autophagy, which is generally considered a cytoprotective response, in that its inhibition frequently promotes apoptotic cells death. Furthermore, it has been shown that conventional chemotherapeutic drugs and radiation alone rarely induce a form of autophagy that leads to cell death. However, there are multiple examples in the literature where newer chemotherapeutic agents, drug combinations or drugs in combination with radiation promote autophagic cell death. This review will describe autophagic cell death induced in breast tumor cells, lung cancer cells as well as glioblastoma, demonstrating that it cannot be concluded that stress induced autophagy is, of necessity, cytoprotective in function.
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DOI：
10.1158/1940-6207.capr-10-0387
发表时间：
2011-07
期刊：
Cancer prevention research (Philadelphia, Pa.)
影响因子：
--
作者：
Chen HY;White E
通讯作者：
White E
影响因子：
11.2
作者：
Apel, Anja;Herr, Ingrid;Mayer, Andreas
通讯作者：
Mayer, Andreas
影响因子：
10.3
作者：
Ito, Hideaki;Aoki, Hiroshi;Kondo, Seiji
通讯作者：
Kondo, Seiji
影响因子：
3.3
作者：
Jung, Chang Hwa;Jun, Chang Bong;Kim, Do-Hyung
通讯作者：
Kim, Do-Hyung
影响因子：
11.2
作者：
Daido, S;Yamamoto, A;Kondo, Y
通讯作者：
Kondo, Y