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细胞外死亡受体途径对失巢凋亡的调控。

Regulation of anoikis by extrinsic death receptor pathways.

机构信息

College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University, Daqing, 163319, China.

Functional Biomaterial Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeonbuk, 56212, Republic of Korea.

出版信息

Cell Commun Signal. 2023 Sep 4;21(1):227. doi: 10.1186/s12964-023-01247-5.

DOI:10.1186/s12964-023-01247-5
PMID:37667281
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10478316/
Abstract

Metastatic cancer cells can develop anoikis resistance in the absence of substrate attachment and survive to fight tumors. Anoikis is mediated by endogenous mitochondria-dependent and exogenous death receptor pathways, and studies have shown that caspase-8-dependent external pathways appear to be more important than the activity of the intrinsic pathways. This paper reviews the regulation of anoikis by external pathways mediated by death receptors. Different death receptors bind to different ligands to activate downstream caspases. The possible mechanisms of Fas-associated death domain (FADD) recruitment by Fas and TNF receptor 1 associated-death domain (TRADD) recruitment by tumor necrosis factor receptor 1 (TNFR1), and DR4- and DR5-associated FADD to induce downstream caspase activation and regulate anoikis were reviewed. This review highlights the possible mechanism of the death receptor pathway mediation of anoikis and provides new insights and research directions for studying tumor metastasis mechanisms. Video Abstract.

摘要

转移性癌细胞在没有附着基质的情况下可以产生抗失巢凋亡能力，并存活下来以对抗肿瘤。失巢凋亡由内源性线粒体依赖性和外源性死亡受体途径介导，研究表明，依赖 caspase-8 的外源性途径似乎比内在途径的活性更为重要。本文综述了死亡受体介导的外源性途径对失巢凋亡的调控。不同的死亡受体与不同的配体结合，从而激活下游的半胱天冬酶。本文综述了 Fas 相关死亡结构域 (FADD) 被 Fas 募集和肿瘤坏死因子受体 1 相关死亡结构域 (TRADD) 被肿瘤坏死因子受体 1 (TNFR1)募集，以及 DR4 和 DR5 相关 FADD 诱导下游半胱天冬酶激活和调节失巢凋亡的可能机制。本综述强调了死亡受体途径介导失巢凋亡的可能机制，为研究肿瘤转移机制提供了新的见解和研究方向。视频摘要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/e019133658b9/12964_2023_1247_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/2e85656b3d09/12964_2023_1247_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/1310fd44bdb6/12964_2023_1247_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/7aea4c642a00/12964_2023_1247_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/53616d255222/12964_2023_1247_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/fbbc9503381d/12964_2023_1247_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/e019133658b9/12964_2023_1247_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/2e85656b3d09/12964_2023_1247_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/1310fd44bdb6/12964_2023_1247_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/7aea4c642a00/12964_2023_1247_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/53616d255222/12964_2023_1247_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/fbbc9503381d/12964_2023_1247_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd6/10478316/e019133658b9/12964_2023_1247_Fig6_HTML.jpg

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