Selective Autophagy in Cancer Development and Therapy

被引：191

作者：

Dikic, Ivan ^{[1
,2
]}

Johansen, Terje ^{[3
]}

Kirkin, Vladimir ^{[1
,2
,4
]}

机构：

[1] Goethe Univ Frankfurt, Frankfurt Inst Mol Life Sci, D-60590 Frankfurt, Germany

[2] Goethe Univ Frankfurt, Inst Biochem 2, D-60590 Frankfurt, Germany

[3] Univ Tromso, Mol Canc Res Grp, Dept Med Biol, Tromso, Norway

[4] Merck KGaA, Darmstadt, Germany

来源：

CANCER RESEARCH | 2010年 / 70卷 / 09期

关键词：

SIGNALING ADAPTER P62; TUMORIGENESIS; PATHWAY; DEGRADATION; UBIQUITIN; BNIP3; MICE;

D O I：

10.1158/0008-5472.CAN-09-4027

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Like other cells in the body, tumor cells depend on the evolutionarily conserved autophagy pathway to survive starvation and stress. Simultaneously, autophagy represents an important tumor-suppressive mechanism. Recent studies have shed new light on this apparent discrepancy and revealed mechanisms by which autophagy can modulate different stages of cancer development. The molecular basis of selectivity in autophagy employs specific receptor molecules, such as p62/SQSTM1, which are able to link autophagy targets and autophagosomal membranes. We discuss the emerging principles of selective autophagy in cancer pathogenesis and treatment. Cancer Res; 70(9); 3431-4. (C) 2010 AACR.

引用

页码：3431 / 3434

页数：4

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