Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo

Toshiyuki Miyashita, Stanislaw Krajewski, Maryla Krajewska, Hong Gang Wang, H. K. Lin, Dan A. Liebermann, Barbara Hoffman, John C. Reed

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Abstract

The p53 tumor suppressor gene product can induce apoptotic cell death through an unknown mechanism. Here we demonstrate that a temperature-sensitive p53 induces temperature-dependent decreases in the expression of the apoptosis-suppressing gene bcl-2 in the murine leukemia cell M1, while simultaneously stimulating increases in the expression of bax, a gene which encodes a dominant-inhibitor of the Bcl-2 protein. Mice deficient in p53 exhibit increases in Bcl-2 and decreases in Bax protein levels in several tissues as determined by immunohistochemical and immunoblot methods. The findings suggest a potential mechanism by which p53 regulates apoptosis, as well as responses to radiation and chemotherapeutic drugs in cancer.

Original languageEnglish (US)
Pages (from-to)1799-1805
Number of pages7
JournalOncogene
Volume9
Issue number6
StatePublished - Jun 1 1994

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All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics
  • Cancer Research

Cite this

Miyashita, T., Krajewski, S., Krajewska, M., Wang, H. G., Lin, H. K., Liebermann, D. A., Hoffman, B., & Reed, J. C. (1994). Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo. Oncogene, 9(6), 1799-1805.