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. 2015 Apr 17;15:301. doi: 10.1186/s12885-015-1300-3

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© Chen et al.; licensee BioMed Central. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Interaction between CIP2A, KRAS genotype and proliferation in the Caco-2 KRAS wild-type cell line. The result of immunoblot and proliferation assay is shown in (a) and (b), respectively. Column 1 vs. 2: CIP2A knockdown by shCIP2A resulted in decreased CIP2A, KRAS, and pERK expression as well as decreased proliferation; Column 1 vs. 3: KRAS overexpression by pCMV6-KRAS G12D resulted in increased KRAS, CIP2A, and pERK expression, as well as increased proliferation; Column 3 vs. 4: in Caco-2 cells with KRAS overexpression by pCMV6-KRAS G12D, knockdown of CIP2A by shCIP2A resulted in decreased CIP2A and KRAS expression. However, it did not cause significantly decreased pERK expression or decreased proliferation (*P < 0.05).