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

    Abstract:

    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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