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自噬在癌症中的作用。

The Roles of Autophagy in Cancer.

机构信息

Medical Science Research Institute, Soonchunhyang University Seoul Hospital, Seoul 04401, Korea.

Department of Biochemistry, Soonchunhyang University College of Medicine, Cheonan 31538, Korea.

出版信息

Int J Mol Sci. 2018 Nov 5;19(11):3466. doi: 10.3390/ijms19113466.


DOI:10.3390/ijms19113466
PMID:30400561
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6274804/
Abstract

Autophagy is an intracellular degradative process that occurs under several stressful conditions, including organelle damage, the presence of abnormal proteins, and nutrient deprivation. The mechanism of autophagy initiates the formation of autophagosomes that capture degraded components and then fuse with lysosomes to recycle these components. The modulation of autophagy plays dual roles in tumor suppression and promotion in many cancers. In addition, autophagy regulates the properties of cancer stem-cells by contributing to the maintenance of stemness, the induction of recurrence, and the development of resistance to anticancer reagents. Although some autophagy modulators, such as rapamycin and chloroquine, are used to regulate autophagy in anticancer therapy, since this process also plays roles in both tumor suppression and promotion, the precise mechanism of autophagy in cancer requires further study. In this review, we will summarize the mechanism of autophagy under stressful conditions and its roles in tumor suppression and promotion in cancer and in cancer stem-cells. Furthermore, we discuss how autophagy is a promising potential therapeutic target in cancer treatment.

摘要

自噬是一种在多种应激条件下发生的细胞内降解过程,包括细胞器损伤、异常蛋白质的存在和营养缺乏。自噬的机制起始于自噬体的形成,自噬体捕获降解成分,然后与溶酶体融合以回收这些成分。自噬的调节在许多癌症中对肿瘤抑制和促进起着双重作用。此外,自噬通过有助于维持干性、诱导复发和对抗癌试剂产生耐药性来调节癌症干细胞的特性。尽管一些自噬调节剂,如雷帕霉素和氯喹,被用于调节抗癌治疗中的自噬,但由于该过程也在肿瘤抑制和促进中发挥作用,因此自噬在癌症中的精确机制需要进一步研究。在这篇综述中,我们将总结应激条件下自噬的机制及其在肿瘤抑制和促进以及癌症干细胞中的作用。此外,我们还讨论了自噬如何成为癌症治疗中有前途的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7688/6274804/6521e755b6d7/ijms-19-03466-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7688/6274804/ba3e18e70906/ijms-19-03466-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7688/6274804/0940a7728760/ijms-19-03466-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7688/6274804/6521e755b6d7/ijms-19-03466-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7688/6274804/ba3e18e70906/ijms-19-03466-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7688/6274804/0940a7728760/ijms-19-03466-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7688/6274804/6521e755b6d7/ijms-19-03466-g003.jpg

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本文引用的文献

[1]
ZC3H13 suppresses colorectal cancer proliferation and invasion via inactivating Ras-ERK signaling.

J Cell Physiol. 2018-10-12

[2]
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Front Cell Dev Biol. 2018-9-10

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Oncol Rep. 2018-8-23

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