title: Protein-bound polysaccharide-K (PSK) induces apoptosis and inhibits proliferation of promyelomonocytic leukemia HL-60 cells.
abstract: Protein-bound polysaccharide-K (PSK) is extracted from Coriolus versicolor (CM101), and is clinically used in combination therapy for gastrointestinal cancer and small cell lung carcinoma. PSK is a biological response modifier (BRM), and its mechanism of action is partly mediated, by modulating host immune systems, such as the activation of immune effector cells and the neutralization of transforming growth factor-beta (TGFβ) activity. Direct inhibition of tumor cell proliferation has been reported as another mechanism, but how PSK induces such an effect remains to be elucidated. Here, the anti-proliferative activity of PSK was examined using seven different human malignant cell lines (WiDr, HT29, SW480, KATOIII, AGS, HL60 and U937), and PSK was found to inhibit the proliferation of HL-60 cells most profoundly. Therefore, HL-60 cells were used to clarify the mechanism of anti-proliferative activity. Caspase-3 activation followed by apoptosis are involved at least in part in the PSK-induced anti-proliferative activity against HL-60 cells.
authors.affiliation: Department of Digestive and General Surgery, Shimane University Faculty of Medicine, 89-1 Enya-cho, Izumo, Shimane 693-8501, Japan. norinori_hirahara@yahoo.co.jp
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Hirahara
authors.forename: Masaki
authors.initials: M
authors.lastname: Fujioka
authors.forename: Takeo
authors.initials: T
authors.lastname: Edamatsu
authors.forename: Ayako
authors.initials: A
authors.lastname: Fujieda
authors.forename: Fujio
authors.initials: F
authors.lastname: Sekine
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Wada
authors.forename: Tsuneo
authors.initials: T
authors.lastname: Tanaka
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects*; D018922:HL-60 Cells; D006801:Humans; D015473:Leukemia, Promyelocytic, Acute / Q000473:pathology*; D011134:Polysaccharides / Q000378:metabolism / Q000494:pharmacology*; D011506:Proteins / Q000378:metabolism*
chemical_list: D011134:Polysaccharides; D011506:Proteins