Over-expression of heparanase promotes proliferation and migration of gallbladder cancer cell line GBC-SD

Objective To investigate the effect of heparanase over-expression on the biological function of gallbladder carcinoma cell line GBC-SD. Methods The heparanase over-expression plasmid vector was constructed and transfected into GBC-SD cells by liposome method. The transfection efficiency was verified...

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Bibliographic Details
Main Author: LIU Zi-xiang, ZHOU Shao-bo, ZHANG Zi-yan
Format: Article
Language:zho
Published: Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College. 2020-02-01
Series:Jichu yixue yu linchuang
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Online Access:http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/a190883.pdf
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Summary:Objective To investigate the effect of heparanase over-expression on the biological function of gallbladder carcinoma cell line GBC-SD. Methods The heparanase over-expression plasmid vector was constructed and transfected into GBC-SD cells by liposome method. The transfection efficiency was verified by RT-qPCR and Western blot. CCK-8 assay, flow cytometry and scratch healing experiment were used to detect the cell proliferation, apoptosis and migration.The expression of syndecan-1, FGF-2 and E-cadherin protein was detected by Western blot. Results The expression of heparanase mRNA(P<0.01) and protein(P<0.05) in gallbladder cancer cell line GBC-SD was significantly increased after transfection.Compared with the control group,the over-expression of heparanase significantly up-regulated the proliferation and migration ability of GBC-SD cells in vitro(P<0.05), down-regulated the level of apoptosis(P<0.05),and increased the expression of FGF-2 protein, while decreasing the expression of syndecan-1(P<0.01) and E-cadherin(P<0.05). Conclusions Over-expression of heparanase promotes the proliferation and migration of gallbladder cancer cell line GBC-SD, and the mechanism may be related to its regulation of E-cadherin through FGF-2.
ISSN:1001-6325