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Published in: BMC Cancer 1/2015

Open Access 01-12-2015 | Research article

CIP2A overexpression induces autoimmune response and enhances JNK signaling pathway in human lung cancer

Authors: Bo Peng, Yurong Chai, Yang Li, Xinxin Liu, Jianying Zhang

Published in: BMC Cancer | Issue 1/2015

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Abstract

Background

Cancerous inhibitor of PP2A (CIP2A) is a recently characterized oncoprotein, which promotes cancer cell proliferation. But the role of CIP2A in lung cancer progression is still not well understood.

Methods

The expression level of CIP2A in lung cancer tissues was examined by immunohistochemistry. CIP2A-associated cell proliferation was performed by knock down or overexpression of CIP2A in lung cancer cells. Phospho-array was used to screen kinase candidates related to expression change of CIP2A. Western-blot and luciferase reporter assay were used to validate phospho-array results.

Results

Overexpression of CIP2A in lung cancer not only triggers immune response in lung cancer patients but also promotes lung cancer cell proliferation. By phospho-array, several kinase candidates were identified, one of which is c-Jun activated kinases (JNK). The knock down of CIP2A decreased JNK phosphorylation, and the phosphorylation of downstream transcriptional factors, ATF2 and c-Jun, whose transcriptional activity were decreased as well. Furthermore, the expression level of CIP2A also affected the phosphorylation of the upstream kinase of JNK, MKK4/MKK7. At last, treatment with JNK inhibitor partially abolished CIP2A-induced cell proliferation.

Conclusion

CIP2A is a tumor-associated autoantigen in lung cancer, which promote lung cancer proliferation partially through MKK4/7-JNK signaling pathway.
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Metadata
Title
CIP2A overexpression induces autoimmune response and enhances JNK signaling pathway in human lung cancer
Authors
Bo Peng
Yurong Chai
Yang Li
Xinxin Liu
Jianying Zhang
Publication date
01-12-2015
Publisher
BioMed Central
Published in
BMC Cancer / Issue 1/2015
Electronic ISSN: 1471-2407
DOI
https://doi.org/10.1186/s12885-015-1899-0

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