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Antibody neutralization of cell-surface gC1qR/HABP1/SF2-p32 prevents lamellipodia formation and tumorigenesis

Authors
Kim, Beom-ChanHwang, Hyun-JungAn, Hyoung-TaeLee, HyunPark, Jun-SubHong, JinKo, JesangKim, ChunghoLee, Jae-SeonKo, Young-Gyu
Issue Date
2-8월-2016
Publisher
IMPACT JOURNALS LLC
Keywords
gC1qR; lamellipodia; cell migration; antibody; cancer
Citation
ONCOTARGET, v.7, no.31, pp.49972 - 49985
Indexed
SCIE
SCOPUS
Journal Title
ONCOTARGET
Volume
7
Number
31
Start Page
49972
End Page
49985
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/87838
DOI
10.18632/oncotarget.10267
ISSN
1949-2553
Abstract
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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