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Comment
. 2013 Aug 12;24(2):141-3.
doi: 10.1016/j.ccr.2013.07.019.

The kinase-independent, second life of CDK6 in transcription

Tobias Otto  1 , Piotr Sicinski
Affiliations
Comment

The kinase-independent, second life of CDK6 in transcription

Tobias Otto et al. Cancer Cell. .

Abstract

CDK6 is an oncogenic kinase regulating the cell cycle. In this issue of Cancer Cell, Kollmann and colleagues demonstrate that CDK6 performs a kinase-independent transcriptional function in regulating expression of VEGF-A and p16INK4a. These observations link the cell cycle machinery and angiogenesis and reveal the presence of a fail-safe antiproliferative mechanism.

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Figures

Figure 1
Figure 1. Model of the Function of CDK6 as Regulator of Cell Cycle and Angiogenesis
Regulation of cell cycle and proliferation by CDK6 depends on the functionality of the p16INK4a protein. CDK6 overexpression can either cause cell cycle arrest in a cell with functional p16INK4a by activating p16INK4a transcription in a kinase-independent manner (left) or promote cell cycle progression if p16INK4a function is lost (right). In addition to regulating cell cycle, CDK6 also induces angiogenesis by activating transcription of VEGF-A, a known angiogenic factor, in a kinase-independent manner.
See this image and copyright information in PMC

Comment on

  • A kinase-independent function of CDK6 links the cell cycle to tumor angiogenesis.
    Kollmann K, Heller G, Schneckenleithner C, Warsch W, Scheicher R, Ott RG, Schäfer M, Fajmann S, Schlederer M, Schiefer AI, Reichart U, Mayerhofer M, Hoeller C, Zöchbauer-Müller S, Kerjaschki D, Bock C, Kenner L, Hoefler G, Freissmuth M, Green AR, Moriggl R, Busslinger M, Malumbres M, Sexl V. Kollmann K, et al. Cancer Cell. 2013 Aug 12;24(2):167-81. doi: 10.1016/j.ccr.2013.07.012. Cancer Cell. 2013. PMID: 23948297 Free PMC article.

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