Drug Resistance Updates
Volume 9, Issue 1 , Pages 19-25 , February 2006

Restoring p53-mediated apoptosis in cancer cells: New opportunities for cancer therapy

  • Qiang Yu

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    • Corresponding Author InformationTel.: +65 6478 8127; fax: +65 6478 9003.

Received 23 February 2006 ,Revised 1 March 2006 ,Accepted 1 March 2006.

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    A dual role of GSK-3β inhibitor LY2119301 in modulating p53 response. DNA damaging chemotherapeutic agents activates p53 and induces growth arrest, through the induction of p21, or apoptosis through t

    A dual role of GSK-3β inhibitor LY2119301 in modulating p53 response. DNA damaging chemotherapeutic agents activates p53 and induces growth arrest, through the induction of p21, or apoptosis through the transcription-independent Bax activation. In many cancer cells, p53 activation favors growth arrest instead of apoptosis. LY2119301 can suppress the p53 transcriptional activity and thus reduces p21 induction. In addition, LY2119301 can trigger p53-dependent Bax activation upon damage. This dual function of LY2119301 converts DNA damage induced p53 response from growth arrest to apoptosis.

PII: S1368-7646(06)00019-7

doi: 10.1016/j.drup.2006.03.001

Drug Resistance Updates
Volume 9, Issue 1 , Pages 19-25 , February 2006

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