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Abstract 4801: p90/CIP2A may play a role in regulating the phosphorylation of CREB1 in cancer

Cancerous inhibitor of PP2A (CIP2A) is a tumor-associated autoantigen migrating in SDS-PAGE as a protein of 90kD (also called p90). This protein was shown to be expressed in the mouse embryonic stage but inactivated in adult tissues. It has been shown to inhibit PP2A function thus stabilizing the oncogene c-myc in human malignancies. In the present study, we used two-dimensional electrophoresis-based approach and identified 47 differentially expressed proteins upon the loss of p90/CIP2A in H1299 lung cancer cell line. Among these 47 proteins, 30 proteins have been well documented to be associated with cancer, of which 12 proteins are up-regulated and 18 proteins are down-regulated after knock-down of p90/CIP2A via shRNA. To investigate whether these proteins are associated with any known cancer-related pathway, differentially expressed proteins were analyzed using Pathway Studio bioinformatics software. The resulting data indicated that four possible transcription factors (c-myc, ESR-1, ETS-1 and CREB) may involve in the regulation of the differentially expressed proteins. Further studies showed that down-regulation of p90/CIP2A may affect CREB phosphorylation: treatment with serum induced less phosphorylation of CREB in cells transduced with p90/CIP2A shRNA than the cells tranduced with control shRNA. However, other treatments like KCl and forskolin did not show significant difference between these two groups. We also found that the phosphorylation of the CREB upstream kinase, AKT, was also down-regulated while other kinases p38 and p90RSK was unaffected. These preliminary data imply that p90/CIP2A may target AKT-CREB pathway to promote cell proliferation in a c-myc independent manner. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4801. doi:1538-7445.AM2012-4801