GSF3, a polysaccharide from guava (Psidium guajava']java L.) seeds, inhibits MCF-7 breast cancer cell growth via increasing Bax/Bcl-2 ratio or Fas mRNA expression levels

被引:21
作者
Lin, Hsiao-Chien [1 ]
Lin, Jin-Yuarn [1 ]
机构
[1] Natl Chung Hsing Univ, Dept Food Sci & Biotechnol, 145 Xingda Rd, Taichung 402, Taiwan
关键词
Cancer immunotherapy; Guava seed polysaccharide fraction 3 (GSF3); Pro-(Bax)/anti-apoptotic (Bcl-2) mRNA; APOPTOSIS; ANTITUMOR; BERBERINE; PATHWAY;
D O I
10.1016/j.ijbiomac.2020.06.057
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Guava seed polysaccharide fraction 3 (GSF3) is an immunomodulatory polysaccharide from guava (Psidium guajava L.) seed polysaccharides. However, effects of GSF3 on the growth of breast cancer cells were not understood, yet. To clarify the GSF3 effects on breast cancer cell growth, GSF3 was subjected to treat MCF-7 cells using direct action or indirect immunotherapy using immune cells conditioned media, respectively. The viabilities of MCF-7 cells were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Changes in pro-(Bax)/anti-apoptotic (Bcl-2) and Fas mRNA expression levels in the treated MCF-7 cells were measured using two-step reverse transcription quantitative polymerase chain reaction. Our results showed that GSF3 inhibited MCF-7 cell growth through either direct action or indirect immunotherapy. GSF3 direct action significantly (P < 0.05) decreased Bcl-2 mRNA expression amount but increased pro-(Bax)/anti-apoptotic (Bcl-2) mRNA expression ratios in the treated cells. The splenocytes conditioned media cultured with GSF3 increased Fas mRNA expression amounts in the treated MCF-7 cells. There was a significant negative correlation between Th2-polarized cytokines secreted by immune cells and Fas mRNA expression levels in the corresponding treated MCF-7 cells. Our findings suggested that GSF3 is a potent anti-cancerous polysaccharide by direct action or indirectly modulating immune cell cytokine secretion profiles. (C) 2020 Elsevier B.V. All rights reserved.
引用
收藏
页码:1261 / 1271
页数:11
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