Antibody neutralization of cell-surface gC1qR/HABP1/SF2-p32 prevents lamellipodia formation and tumorigenesis
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Beom-Chan Kim1,2, Hyun-Jung Hwang1,3, Hyoung-Tae An1,2, Hyun Lee1,2, Jun-Sub Park1,2, Jin Hong1,2, Jesang Ko1,2, Chungho Kim1, Jae-Seon Lee3, Young-Gyu Ko1,2
1Tunneling Nanotube Research Center, Korea University, Seoul, 02841, Korea
2Division of Life Sciences, Korea University, Seoul, 02841, Korea
3Department of Molecular Medicine, College of Medicine, Inha University, Incheon, 22212, Korea
Young-Gyu Ko, email: firstname.lastname@example.org
Keywords: gC1qR, lamellipodia, cell migration, antibody, cancer
Received: January 07, 2016 Accepted: May 28, 2016 Published: June 24, 2016
We previously demonstrated that cell-surface gC1qR is a key regulator of lamellipodia formation and cancer metastasis. Here, we screened a monoclonal mouse antibody against gC1qR to prevent cell migration by neutralizing cell-surface gC1qR. The anti-gC1qR antibody prevented growth factor-stimulated lamellipodia formation, cell migration and focal adhesion kinase activation by inactivating receptor tyrosine kinases (RTKs) in various cancer cells such as A549, MDA-MB-231, MCF7 and HeLa cells. The antibody neutralization of cell-surface gC1qR also inhibited angiogenesis because the anti-gC1qR antibody prevented growth factor-stimulated RTK activation, lamellipodia formation, cell migration and tube formation in HUVEC. In addition, we found that A549 tumorigenesis was reduced in a xenograft mouse model by following the administration of the anti-gC1qR antibody. With these data, we can conclude that the antibody neutralization of cell-surface gC1qR could be a good therapeutic strategy for cancer treatment.
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