A Kinase-Independent Function of CDK6 Links the Cell Cycle to Tumor Angiogenesis

(Cancer Cell 24, 167–181; August 12, 2013) In the original Figure 3C, the files from patient B were accidentally uploaded twice for patient B and patient C. The corrected files for patient C have been corrected in the figure below. The authors apologize for any confusion this may have caused the readers. A Kinase-Independent Function of CDK6 Links the Cell Cycle to Tumor AngiogenesisKollmann et al.Cancer CellAugust 12, 2013In BriefIn contrast to its close homolog CDK4, the cell cycle kinase CDK6 is expressed at high levels in lymphoid malignancies. In a model for p185BCR-ABL+ B-acute lymphoid leukemia, we show that CDK6 is part of a transcription complex that induces the expression of the tumor suppressor p16INK4a and the pro-angiogenic factor VEGF-A. This function is independent of CDK6’s kinase activity. High CDK6 expression thus suppresses proliferation by upregulating p16INK4a, providing an internal safeguard. However, in the absence of p16INK4a, CDK6 can exert its full tumor-promoting function by enhancing proliferation and stimulating angiogenesis. Full-Text PDF Open Access