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自噬作为乳腺肿瘤细胞辐射增敏的一种机制。

Autophagy as a mechanism of radiation sensitization in breast tumor cells.

作者信息

Gewirtz David A

机构信息

Department of Pharmacology and Toxicology, Virginia Commonwealth University, Massey Cancer Center, Virginia 23298, USA.

出版信息

Autophagy. 2007 May-Jun;3(3):249-50. doi: 10.4161/auto.3723. Epub 2007 May 19.

Abstract

Current studies to define the mechanism by which vitamin D3 and analogs of vitamin D3 enhance the response to ionizing radiation in breast tumor cells suggest that these effects are mediated, in large part, through the promotion of autophagic cell death. The residual surviving cell population remains in a senescent, growth arrested state, with minimal recovery of proliferative capacity. It is becoming evident that pathways other than or in addition to apoptosis, including senescence arrest, mitotic catastrophe and autophagy, contribute to loss of self-renewal capacity in tumor cells exposed to chemotherapeutic drugs and ionizing radiation. How and why the cell chooses a particular growth arrest and/or cell death pathway remains a puzzle to be solved.

摘要

目前旨在确定维生素D3及其类似物增强乳腺肿瘤细胞对电离辐射反应机制的研究表明,这些作用在很大程度上是通过促进自噬性细胞死亡来介导的。残余的存活细胞群体处于衰老、生长停滞状态,增殖能力几乎没有恢复。越来越明显的是,除凋亡之外或与之并存的其他途径,包括衰老停滞、有丝分裂灾难和自噬,都有助于导致暴露于化疗药物和电离辐射的肿瘤细胞自我更新能力的丧失。细胞如何以及为何选择特定的生长停滞和/或细胞死亡途径仍是有待解决的谜题。

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