Effects of polysaccharides from Ginkgo biloba on proliferation of 4T1 breast cancer cells and expression of GLUT family genes
10.3969/j.issn.1001-1978.2018.09.022
- VernacularTitle:银杏多糖对小鼠乳腺癌4T1细胞增殖及GLUT家族基因表达的影响
- Author:
Ping CHANG
1
;
Yan XU
;
Da-Yu ZHOU
;
Jia-Di WU
;
Shi-Liang MA
Author Information
1. 沈阳农业大学生物科学技术学院
- Keywords:
Ginkgo polysaccharides;
4T1 breast canc-er cell;
proliferation;
apoptosis;
glucose transporters;
glucose transporter 1;
energy metabolism
- From:
Chinese Pharmacological Bulletin
2018;34(9):1301-1307
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effects of polysac-charides from Ginkgo biloba on the proliferation, apop-tosis of mouse 4T1 breast cancer cells and the possible mechanism. Methods 4T1 cells in logarithmic growth phase were treated with polysaccharides from Ginkgo biloba of different concentrations. The effect of poly-saccharides from Ginkgo biloba on inhibition of prolif-eration and cytotoxicity of 4T1 cells was determined by MTT assay and trypan blue exclusion assay respective-ly. The apoptotic effect of polysaccharides from Ginkgo biloba on 4T1 cells was detected by DAPI staining. qRT-PCR experiments were carried out for the detec-tion of gene expressions of the glucose transporter fami-ly upon the treatment with the polysaccharides from Ginkgo biloba. Results Polysaccharides from either Ginkgo biloba leaf or Ginkgo biloba exocarp significant-ly inhibited the proliferation of 4T1 cells in a dose-and time-dependent manner. Moreover, with the increasing doses of polysaccharides, cell viability decreased, ac-companied by the increased cell cytotoxicity and apop-tosis. qRT-PCR results showed that polysaccharides from Ginkgo biloba significantly reduced glucose trans-porter 1 gene expression. Conclusions Polysaccha-rides from Ginkgo biloba can both inhibit 4T1 cell pro-liferation and induce cell apoptosis, and by regulating glucose transporter family gene expression, it interfered with cell energy metabolism, which infers that the effects of cell proliferation inhibition as well the apopto-sis induction might be due to the regulation of glucose transporter family gene expression.
