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. Author manuscript; available in PMC: 2014 Nov 15.
Published in final edited form as: Cancer Res. 2013 Sep 26;73(22):10.1158/0008-5472.CAN-13-1002. doi: 10.1158/0008-5472.CAN-13-1002

Figure 7.

Figure 7

In unperturbed cancer cells, DNA-PK activity promotes constitutive Chk1 serine 345 phosphorylation and CIP2A expression. (Left panel) Constitutively active Chk1 together with Claspin, promotes CIP2A gene transcriptio and protein expression. CIP2A in turn inhibits PP2A tumor suppressor activity and thereby increases activity/expression of oncogenic PP2A targets (such as MYC). (Right panel) Inhibition of the Chk1 activity by means of cancer therapy results in increase in PP2A activity, dephosphorylation of PP2A target proteins, and inhibition of cancer cell viability. Inactive molecules and functions are shown in grey.