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

Beom Chan Kim, Hyun Jung Hwang, Hyoung Tae An, Hyun Lee, Jun Sub Park, Jin Hong, Je Sang Ko, Chungho Kim, Jae Seon Lee, Young-Gyu Ko

Research output: Contribution to journalArticle

10 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)49972-49985
Number of pages14
JournalOncotarget
Volume7
Issue number31
DOIs
Publication statusPublished - 2016

Keywords

  • Antibody
  • Cancer
  • Cell migration
  • GC1qR
  • Lamellipodia

ASJC Scopus subject areas

  • Oncology

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