Galectin-3 Promotes Cell Proliferation and Attenuates Cytotoxic Effect of Paclitaxel via ERK Signaling Pathway in Gastric Cancer Cells.

Research Project

Project/Area Number	15K08959
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Gastroenterology
Research Institution	Juntendo University
Principal Investigator	SERIZAWA Nobuko 順天堂大学, 医学部, 非常勤講師 (00445545)
Co-Investigator(Kenkyū-buntansha)	永原章仁順天堂大学, 医学部, 教授 (00266040) 北條麻理子順天堂大学, 医学部, 准教授 (60372934)
Project Period (FY)	2015-04-01 – 2018-03-31
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000) Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000) Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords	ガレクチン-3 / 胃癌 / パクリタキセル / ERKシグナル伝達系
Outline of Final Research Achievements	Our aim in this study is to assess whether silencing of galectin-3 contributes to the inhibition of gastric cancer cell proliferation and enhances the effect of paclitaxel through ERK (Extracellular Signal-regulated Kinase) signaling pathway. The proliferating cells were decreased in galectin-3 siRNA transfected cells compared to control cells. Western blot showed that phosphorylation of ERK was reduced in galectin-3 siRNA transfected cells. Cell proliferation in galectin-3 siRNA transfected cells was decreased compared to control cells in the presence of paclitaxel (TXL). Western blot showed that phosphorylation of ERK was reduced in galectin-3 siRNA/TXL combination compared to scrambled siRNA/TXL combination. These results indicate that silencing of galectin-3 downregulates ERK signaling pathway and enhances the effect of TXL, leading to synergistic inhibition of cell proliferation in gastric cancer.