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Prunella vulgaris polysaccharide inhibits growth and migration of breast carcinoma-associated fibroblasts by suppressing expression of basic fibroblast growth factor.
Chinese Journal of Integrative Medicine 2016 September 2
OBJECTIVE: To study the effects of Prunella vulgaris polysaccharide (PVP) on human breast carcinoma-associated fibroblasts (CAFs).
METHODS: Cell viability was detected by 3-[4,5-dimethylthiazol-2-yl]-2,5-(3-carboxymethoxyphenyl)-2-4-sulfophenyl)-2H-tetrazolium (MTS) assay. Wound healing experiment and transwell migration assay were used to investigate the anti-migration effects. Flow cytometry was applied to detect cell apoptosis and cell cycle distribution. Reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay were used to detect the expression of basic fifibroblast growth factor (bFGF) in CAFs. Culture SKBr-3 with CAFs conditioned medium (CAFs-CM) to evaluate the indirect function on the proliferation of breast cancer SKBr-3 cells.
RESULTS: PVP inhibited the viability of CAFs by inducing apoptosis (P <0.01) and arresting cell cycle (P <0.01). It also inhibited the migration of CAFs (P <0.01). bFGF promoted CAFs proliferation (P <0.01) and migration (P <0.01), protected CAFs from apoptosis (P <0.05) and reduced G0 phase to 49.06% (P <0.01). However, these effects of bFGF on CAFs could be abrogated by PVP. Culturing SKBr-3 with CAFs-CM, PVP could inhibit the viability of breast cancer SKBr-3 cells indirectly. Moreover, PVP reduced the mRNA expression (P <0.01) and protein secretion of bFGF (P <0.01) in CAFs.
CONCLUSION: PVP could exert an anti-cancer effect on breast CAFs by inhibiting bFGF expression, thus inhibiting the growth of breast cancer SKBr-3 cells indirectly.
METHODS: Cell viability was detected by 3-[4,5-dimethylthiazol-2-yl]-2,5-(3-carboxymethoxyphenyl)-2-4-sulfophenyl)-2H-tetrazolium (MTS) assay. Wound healing experiment and transwell migration assay were used to investigate the anti-migration effects. Flow cytometry was applied to detect cell apoptosis and cell cycle distribution. Reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay were used to detect the expression of basic fifibroblast growth factor (bFGF) in CAFs. Culture SKBr-3 with CAFs conditioned medium (CAFs-CM) to evaluate the indirect function on the proliferation of breast cancer SKBr-3 cells.
RESULTS: PVP inhibited the viability of CAFs by inducing apoptosis (P <0.01) and arresting cell cycle (P <0.01). It also inhibited the migration of CAFs (P <0.01). bFGF promoted CAFs proliferation (P <0.01) and migration (P <0.01), protected CAFs from apoptosis (P <0.05) and reduced G0 phase to 49.06% (P <0.01). However, these effects of bFGF on CAFs could be abrogated by PVP. Culturing SKBr-3 with CAFs-CM, PVP could inhibit the viability of breast cancer SKBr-3 cells indirectly. Moreover, PVP reduced the mRNA expression (P <0.01) and protein secretion of bFGF (P <0.01) in CAFs.
CONCLUSION: PVP could exert an anti-cancer effect on breast CAFs by inhibiting bFGF expression, thus inhibiting the growth of breast cancer SKBr-3 cells indirectly.
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