Caspase 3-mediated stimulation of tumor cell repopulation during cancer radiotherapy

Qian Huang, Fang Li, Xinjian Liu, Wenrong Li, Wei Shi, Fei Fei Liu, Brian O'Sullivan, Zhimin He, Yuanlin Peng, Aik Choon Tan, Ling Zhou, Jingping Shen, Gangwen Han, Xiao Jing Wang, Jackie Thorburn, Andrew Thorburn, Antonio Jimeno, David Raben, Joel S. Bedford, Chuan Yuan Li

Research output: Contribution to journalArticlepeer-review

631 Citations (Scopus)


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 E 2 (PGE 2), 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.

Original languageEnglish
Pages (from-to)860-866
Number of pages7
JournalNature Medicine
Issue number7
Publication statusPublished - 2011 Jul

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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