Cancer Institute A national cancer institute
designated cancer center

Dean W. Felsher

Publication Details

  • STK38 is a critical upstream regulator of MYC's oncogenic activity in human B-cell lymphoma. Oncogene Bisikirska, B. C., Adam, S. J., Alvarez, M. J., Rajbhandari, P., Cox, R., Lefebvre, C., Wang, K., Rieckhof, G. E., Felsher, D. W., Califano, A. 2012


    The MYC protooncogene is associated with the pathogenesis of most human neoplasia. Conversely, its experimental inactivation elicits oncogene addiction. Besides constituting a formidable therapeutic target, MYC also has an essential function in normal physiology, thus creating the need for context-specific targeting strategies. The analysis of post-translational MYC activity modulation yields novel targets for MYC inactivation. Specifically, following regulatory network analysis in human B-cells, we identify a novel role of the STK38 kinase as a regulator of MYC activity and a candidate target for abrogating tumorigenesis in MYC-addicted lymphoma. We found that STK38 regulates MYC protein stability and turnover in a kinase activity-dependent manner. STK38 kinase inactivation abrogates apoptosis following B-cell receptor activation, whereas its silencing significantly decreases MYC levels and increases apoptosis. Moreover, STK38 knockdown suppresses growth of MYC-addicted tumors in vivo, thus providing a novel viable target for treating these malignancies.Oncogene advance online publication, 26 November 2012; doi:10.1038/onc.2012.543.

    View details for PubMedID 23178486

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