Non-lethal outcomes of engaging regulated cell death pathways in cancer

被引:0
作者
Halime Kalkavan
Sebastian Rühl
Jeremy J. P. Shaw
Douglas R. Green
机构
[1] St Jude Children’s Research Hospital,Department of Immunology
[2] University Hospital Essen,West German Cancer Center, Department of Medical Oncology
[3] Partner Site University Hospital Essen,German Cancer Consortium (DKTK)
[4] T3 Pharmaceuticals AG,undefined
来源
Nature Cancer | 2023年 / 4卷
关键词
D O I
暂无
中图分类号
学科分类号
摘要
Regulated cell death (RCD) is essential for successful systemic cancer therapy. Yet, the engagement of RCD pathways does not inevitably result in cell death. Instead, RCD pathways can take part in diverse biological processes if the cells survive. Consequently, these surviving cells, for which we propose the term ‘flatliners’, harbor important functions. These evolutionarily conserved responses can be exploited by cancer cells to promote their own survival and growth, with challenges and opportunities for cancer therapy.
引用
收藏
页码:795 / 806
页数:11
相关论文
共 279 条
[31]  
Hata AN(2009)Co-operative and hierarchical binding of c-FLIP and caspase-8: a unified model defines how c-FLIP isoforms differentially control cell fate Cancer Lett. 281 549-119
[32]  
Lockshin RA(2015)Caspase-8 in cancer biology and therapy Cell Death Differ. 22 5530-714
[33]  
Zakeri Z(2021)The role of CD95 and CD95 ligand in cancer FEBS J. 288 26-448
[34]  
Li P(2015)The multifaceted role of TRAIL signaling in cancer and immunity Semin. Cell Dev. Biol. 39 2186-454
[35]  
Lakhani SA(2013)Fas and TRAIL ‘death receptors’ as initiators of inflammation: implications for cancer Mol. Biol. Cell 24 2240-3250
[36]  
Bedoui S(2012)Cells surviving fractional killing by TRAIL exhibit transient but sustainable resistance and inflammatory phenotypes Mol. Biol. Cell 23 9015-725
[37]  
Herold MJ(2015)Cell survival, DNA damage, and oncogenic transformation after a transient and reversible apoptotic response Sci. Rep. 5 112-601
[38]  
Strasser A(2005)In vivo CaspaseTracker biosensor system for detecting anastasis and non-apoptotic caspase activity Nat. Chem. Biol. 1 700-218
[39]  
Du C(2010)Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury Nat. Rev. Mol. Cell Biol. 11 432-883
[40]  
Fang M(2011)Molecular mechanisms of necroptosis: an ordered cellular explosion Mol. Cell 43 411-109