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New paper out on a novel function of CDK6 in tumor angiogenesis

Richard Moriggl and Lukas Kenner contributed to a study lead by Veronika Sexl of the University of Veterinary Medicine Vienna,  which was now published in the prestigious journal Cancer Cell

The report describes a novel function for the cell cycle kinase CDK6, which is expressed at high levels in lymphoid malignancies. In a mouse model for lymphoid leukemia CDK6 is part of a transcription complex, which does not require the enzymatic function of CDK6. A transcription factor complex forms with STAT3 that induces the expression of the tumor suppressor p16INK4a and the pro-angiogenic factor VEGF-A. But if the tumor suppressor is lost through mutation, CDK6 can exert its full tumor-promoting function by enhancing proliferation and stimulating angiogenesis. The finding that CDK6 connects cell-cycle progression to angiogenesis confirms CDK6’s central role in hematopoietic malignancies and could underlie the selection pressure to upregulate CDK6 and silence p16INK4a.

 

The cell cycle dependent kinase 6 (CDK6) has functions, which are kinase dependent as well as independent.