galectin-3 facilitates cell motility in gastric cancer by up-regulating protease-activated receptor-1(par-1) and matrix metalloproteinase-1(mmp-1)galectin-3促进胃癌细胞活性的调控protease-activated receptor-1(par-1)和矩阵metalloproteinase-1(金属蛋白酶- 1).pdfVIP

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galectin-3 facilitates cell motility in gastric cancer by up-regulating protease-activated receptor-1(par-1) and matrix metalloproteinase-1(mmp-1)galectin-3促进胃癌细胞活性的调控protease-activated receptor-1(par-1)和矩阵metalloproteinase-1(金属蛋白酶- 1).pdf

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galectin-3 facilitates cell motility in gastric cancer by up-regulating protease-activated receptor-1(par-1) and matrix metalloproteinase-1(mmp-1)galectin-3促进胃癌细胞活性的调控protease-activated receptor-1(par-1)和矩阵metalloproteinase-1(金属蛋白酶- 1)

Galectin-3 Facilitates Cell Motility in Gastric Cancer by Up-Regulating Protease-Activated Receptor-1(PAR-1) and Matrix Metalloproteinase-1(MMP-1) 1,3 1 1 2 1 3 Seok-Jun Kim , Ji-Young Shin , Kang-Duck Lee , Young-Ki Bae , Il-Ju Choi , Seok Hee Park , Kyung- Hee Chun1* 1 Gastric Cancer Branch, Division of Translational and Clinical Research I, National Cancer Center Research Institute and Hospital, Jungbalsan-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do, Republic of Korea, 2 Cancer Experimental Recourses Branch, Division of Cancer Biology, National Cancer Center, Ilsandong-gu, Goyang-si, Gyeonggi-do, Republic of Korea, 3 Department of Biological Science, Sungkyunkwan University, Jangan-gu, Suwon-si, Gyeonggi-do, Republic of Korea Abstract Background: Galectin-3 is known to regulate cancer metastasis. However, the underlying mechanism has not been defined. Through the DNA microarray studies after galectin-3 silencing, we demonstrated here that galectin-3 plays a key role in up- regulating the expressions of protease-activated receptor-1(PAR-1) and matrix metalloproteinase-1(MMP-1) PAR-1 thereby promoting gastric cancer metastasis. Methodology/Principal Findings: We examined the expression levels of Galectin-3, PAR-1, and MMP-1 in gastric cancer patient tissues and also the effects of silencing these proteins with specific siRNAs and of over-expressing them using specific lenti-viral constructs. We also employed zebrafish embryo model for analysis of in vivo gastric cancer cell invasion. These studies demonstrated that: a) galectin-3 silencing decreases the expression of PAR-1. b) galectin-3 over-expression increases cell migration and invasion and this increase can be reversed by PAR-1 silencing, indicating