Caspase 3-mediated stimulation of tumor cell repopulation during cancer radiotherapy
By Qian Huang, Fang Li, Xinjian Liu, Wenrong Li, W. Shi, Fei-Fei Liu, B. O'Sullivan, Zhiming He, Yuanlin Peng, Aik Choon Tan and 10 more. Nature Medicine, 2011
842 citations recorded by the source corpus.
In cancer treatment, apoptosis is a well-recognized cell death mechanism through which cytotoxic agents kill tumor cells. Here we report that dying tumor cells use the apoptotic process to generate potent growth-stimulating signals to stimulate the repopulation of tumors undergoing radiotherapy. Furthermore, activated caspase 3, a key executioner in apoptosis, is involved in the growth stimulation. One downstream effector that caspase 3 regulates is prostaglandin E2 (PGE2), which can potently stimulate growth of surviving tumor cells. Deficiency of caspase 3 either in tumor cells or in tumor stroma caused substantial tumor sensitivity to radiotherapy in xenograft or mouse tumors. In human subjects with cancer, higher amounts of activated caspase 3 in tumor tissues are correlated with markedly increased rate of recurrence and death. We propose the existence of a cell death–induced tumor repopulation pathway in which caspase 3 has a major role.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/b0f42f92e6fd4522affe821177b96fe1f3ef7880
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Citations in the corpus
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “positively or negatively regulate the emission of multiple DAMPs from dying cells, including immunostimulatory [229] as well as immunosuppressive [230] factors.”
- Apoptotic Caspases Suppress mtDNA-Induced STING-Mediated Type I IFN Production (2014, neutral): “, prostaglandin-induced tumor cell repopulation [Huang et al., 2011] and AMPA receptor internalization [Li et al.”