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PLoS One. 2014 May 21;9(5):e97578. doi: 10.1371/journal.pone.0097578. eCollection 2014.

IQGAP3 promotes EGFR-ERK signaling and the growth and metastasis of lung cancer cells.

Author information

1
Department of Immunology, School of Basic Medical Sciences, Key Laboratory of Medical Immunology of Ministry of Public Health, Peking University Health Science Center, Beijing, P. R. China.

Abstract

Proteins of the IQGAP family display complicated and often contradictory activities in tumorigenesis. IQGAP1 has well documented oncogenic potential and IQGAP2 has putative tumor-suppressive function. IQGAP3 is the latest addition to this family and its role in cancer development remains to be defined. Here we demonstrate IQGAP3 expression is markedly increased in lung cancer tissues at both mRNA and protein levels. Overexpression of IQGAP3 promoted tumor cell growth, and migration and invasion, whereas knockdown of IQGAP3 exhibited opposite effects. Moreover, suppression of IQGAP3 in a lung cancer cell line caused a reduction in the tumorigenicity of these cells in lung tissue after intravenous injection. Furthermore, we showed that IQGAP3 is able to interact with ERK1 and enhance its phosphorylation following treatment with EGF. These data suggest that IQGAP3 may contribute to the pathogenesis of lung cancer by modulating EGFR-ERK signaling.

PMID:
24849319
PMCID:
PMC4029748
DOI:
10.1371/journal.pone.0097578
[Indexed for MEDLINE]
Free PMC Article

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