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作 者:Emma Guilbaud Lorenzo Galluzzi
机构地区:[1]Department of Radiation Oncology,Weill Cornell Medical College,New York,NY,USA [2]Sandra and Edward Meyer Cancer Center,New York,NY,USA [3]Caryl and Israel Englander Institute for Precision Medicine,New York,NY,USA
出 处:《Cell Research》2023年第2期93-94,共2页细胞研究(英文版)
摘 要:While widespread mitochondrial outer membrane permeabilization(MOMP)generally seals the fate of stressed cancer cells as it elicits caspase-dependent mechanisms that regulate the kinetics and immunological manifestations of cell death,partial MOMP driving sublethal caspase activation has been associated with cancer cell survival in the context of accrued genomic instability.Recent findings delineate a novel caspase-independent mechanism linking sublethal MOMP to the acquisition of a persister phenotype coupled to chemoresistance and accrued metastatic potential.
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