Potential mechanism of mycelium polysaccharide from Pholiota dinghuensis Bi in regulating the proliferation and apoptosis of human breast cancer MCF-7 cells through p38/MAPK pathway

• PDP-3 inhibited the proliferation of human breast estrogen-dependent cancer MCF-7 cells.
• PDP-3 regulated proteins expression in the proliferation and cell cycle in MCF-7 cells.
• PDP-3 regulated expression of ERα and proteins involved in the apoptosis in MCF-7 cells.
• P38/MAPK signal transduction pathway was the potential mechanism of PDP-3 in regulating both of proliferation and apoptosis.

The antiproliferative and apoptosis-inducing activities of an acidic polysaccharides fraction from Pholiota dinghuensis Bi mycelium (PDP-3) against human breast cancer MCF-7 cells were investigated. As a result, PDP-3 displayed a significant prevention of cell growth towards MCF-7 cells, with an EC50 value of 38.35 µg/mL. Furthermore, PDP-3 induced significant apoptosis towards MCF-7 cells. From Western blot results, up-regulated p21 and down-regulated cyclin D1, CDK4 and PCNA, up-regulated Bax and down-regulated Bcl-2, caspase-9 and caspase-3 were found in the protein expressions of MCF-7 cells. In MCF-7 cells treated with PDP-3, down-regulated TRAF2 and up-regulated ASK1, phosphorylated of p38 and p53 were also found. Notably, PDP-3 treatment represented a significant decrease in both nuclear and cytoplasmic expression of ERα in MCF-7 cells. Therefore, p38/MAPK signal transduction pathway was the potential mechanism of PDP-3 in regulating both cell proliferation and apoptosis in oestrogen-dependent human breast cancer MCF-7 cells.