Molecular mechanism in direct effect of VEGF onto breast cancer cells

2015 Fiscal Year Final Research Report

• Project/Area Number: 24390301
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: General surgery
• Research Institution: Kyoto University
• Principal Investigator: SATO FUMIAKI 京都大学, 医学(系)研究科(研究院), 准教授 (20467426)
• Co-Investigator(Kenkyū-buntansha): TOI Masakazu 京都大学, 大学院医学研究科, 教授 (10207516) ; UENO Takayuki 京都大学, 大学院医学研究科, 助教 (40452362) ; SAJI Shigehira 京都大学, 大学院医学研究科, 特定准教授 (80446567)
• Co-Investigator(Renkei-kenkyūsha): MIKAMI Yoshiki 京都大学, 大学院医学研究科, 准教授 (90248245)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: 乳癌 / VEGF / NRP1 / 細胞運動

Outline of Final Research Achievements

The purpose of this study is to elucidate the molecular mechanism of direct effect by VEGF to breast cancer cells. In this study, VEGF signal into MB-231 cells was blocked by VEGF-knockout and soluble NRP1 expression. Experiments using these cells showed that MB-231 cells are directly stimulated by VEGF via NRP1 not VEGFR, which contributes to spindle-like morphology formation and higher cell migration activity of breast cancer cells. According to microarray-based gene expression analysis of these cells, VEGF/NRP1 signaling modulates the expression of factor X that is negative regulator of cdc42. In summary, VEGF changes morphology of MB-231 cells and stimulates motility of MB-231 cells by VEGF/NRP1/factor X/cdc42 signaling pathway.

Free Research Field

乳腺外科