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不依赖半胱天冬酶的细胞死亡不会引发黑色素瘤癌细胞的增殖反应。

Caspase-independent cell death does not elicit a proliferative response in melanoma cancer cells.

作者信息

Roumane Ahlima, Berthenet Kevin, El Fassi Chaïmaa, Ichim Gabriel

机构信息

INSERM 1052, CNRS 5286, Cancer Research Center of Lyon (CRCL), Lyon, France.

LabEx DEVweCAN, Université de Lyon, Lyon, France.

出版信息

BMC Cell Biol. 2018 Jul 4;19(1):11. doi: 10.1186/s12860-018-0164-1.

DOI:10.1186/s12860-018-0164-1
PMID:29973136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6030751/
Abstract

BACKGROUND

Apoptosis, the most well-known type of programmed cell death, can induce in a paracrine manner a proliferative response in neighboring surviving cells called apoptosis-induced proliferation (AiP). While having obvious benefits when triggered in developmental processes, AiP is a serious obstacle in cancer therapy, where apoptosis is frequently induced by chemotherapy. Therefore, in this study, we evaluated the capacity of an alternative type of cell death, called caspase-independent cell death, to promote proliferation.

RESULTS

Using a novel in vitro isogenic cellular model to trigger either apoptosis or caspase-independent cell death, we found that the later has no obvious compensatory proliferation effects on neighboring cells.

CONCLUSIONS

This study enforces the idea that alternative types of cell death such as caspase-independent cell death could be considered to replace apoptosis in the context of cancer treatment.

摘要

背景

凋亡是最广为人知的程序性细胞死亡类型,它能够以旁分泌的方式诱导邻近存活细胞产生增殖反应,即凋亡诱导增殖(AiP)。虽然在发育过程中触发AiP有明显益处,但在癌症治疗中却是一个严重障碍,因为化疗常常会诱导凋亡。因此,在本研究中,我们评估了另一种细胞死亡类型——即不依赖半胱天冬酶的细胞死亡——促进增殖的能力。

结果

使用一种新型的体外同基因细胞模型来触发凋亡或不依赖半胱天冬酶的细胞死亡,我们发现后者对邻近细胞没有明显的代偿性增殖作用。

结论

本研究强化了这样一种观点,即在癌症治疗的背景下,可以考虑用诸如不依赖半胱天冬酶的细胞死亡等其他类型的细胞死亡来替代凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd3/6030751/1050bb4a716f/12860_2018_164_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd3/6030751/2e01e96bef11/12860_2018_164_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd3/6030751/e096acd605b5/12860_2018_164_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd3/6030751/1050bb4a716f/12860_2018_164_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd3/6030751/2e01e96bef11/12860_2018_164_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd3/6030751/e096acd605b5/12860_2018_164_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cd3/6030751/1050bb4a716f/12860_2018_164_Fig3_HTML.jpg

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本文引用的文献

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Caspase-independent cell death: An anti-cancer double whammy.非半胱天冬酶依赖性细胞死亡:抗癌的双重打击。
Cell Cycle. 2018;17(3):269-270. doi: 10.1080/15384101.2017.1408229. Epub 2018 Feb 19.
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Mitochondrial permeabilization engages NF-κB-dependent anti-tumour activity under caspase deficiency.在半胱天冬酶缺乏的情况下,线粒体通透性改变会引发核因子κB依赖性抗肿瘤活性。
重组人促红细胞生成素可降低三维培养的MCF-7乳腺癌细胞的活力,且不激活半胱天冬酶。
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The Great Escape: The Power of Cancer Stem Cells to Evade Programmed Cell Death.《大逃脱:癌症干细胞逃避程序性细胞死亡的能力》
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Apoptosis - Fueling the oncogenic fire.细胞凋亡——点燃致癌之火。
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