IQGAP3 promotes EGFR-ERK signaling and the growth and metastasis of lung cancer cells.
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.
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.
Ying
Y
Yang
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.
Wei
W
Zhao
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.
Qing-Wen
QW
Xu
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.
Xiao-Song
XS
Wang
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.
Yu
Y
Zhang
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.
Jun
J
Zhang
D063646:Carcinogenesis; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D066246:ErbB Receptors / Q000378:metabolism*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D020690:GTPase-Activating Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D055785:Gene Knockdown Techniques; D006801:Humans; D008175:Lung Neoplasms / Q000473:pathology*; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D010766:Phosphorylation; D015398:Signal Transduction; D015854:Up-Regulation
D020690:GTPase-Activating Proteins; C000594387:IQGAP3 protein, human; D066246:ErbB Receptors; D048049:Extracellular Signal-Regulated MAP Kinases