Abstract: Objective: The study investigated the inhibitory effect of the ethyl acetate fraction of Pleurotus ferulatus triterpenoid (PFTP-E) on the proliferation of human esophageal carcinoma Eca109 cells and the possible underlying mechanism. Methods: Cell proliferation in vitro was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Hoechst 33258 staining was used to observe cell apoptosis. Flow cytometry was used to assess cell proliferation, cycle, apoptosis, mitochondrial membrane potential and intracellular reactive oxygen species (ROS). The effects of PFTP-E on the expression of the apoptosis-related proteins Bcl2, Bax, poly ADP-ribose polymerase (PARP), caspase 3 and caspase 9; the cell cycle-related protein cyclin B1; the endoplasmic reticulum stress-related proteins eukaryotic initiation factor 2α (eIF2α) and CHOP; and mitogen-activated protein kinase (MAPK) signaling pathway-related proteins were detected by Western blot. Results: PFTP-E inhibited the proliferation of Eca109 cells in both a time and dose-dependent manner, blocked the cell cycle in G2/M phase and induced cell apoptosis. Meanwhile, PFTP-E decreased mitochondrial membrane potential and increased intracellular ROS production. In addition, PFTP-E could up-regulate the expression of cytochrome c, Bax, p-eIF2α and CHOP, down-regulate the expression of Bcl2 and cyclin B1, significantly increase cleaved-PARP, cleaved-caspase 3 and cleaved-caspase 9 expression levels, induce endoplasmic reticulum stress and activate the MAPK/JNK signaling pathway. Conclusion: PFTP-E can effectively induce apoptosis, and the underlying anti-tumor mechanism is related to mitochondrial damage, cell cycle block, endoplasmic reticulum stress.

Key words: Pleurotus ferulae, triterpenoid, Eca109 cells, apoptosis