title: PSK induces apoptosis through the inhibition of activated STAT3 in human             esophageal carcinoma cells.
abstract: PSK, a protein-bound polysaccharide, is widely used in Japan as an immunopotentiating             biological response modifier for cancer patients. PSK exerts antitumor activities             through stimulation of the host's immune response; however, few studies have addressed             the direct actions of PSK on tumor cells. Recently, it has been found that STAT3             is aberrantly activated in various types of malignancies, and plays a crucial             role in tumor cell proliferation and survival. In the present study, STAT3 was             constitutively activated in KYSE170 and TE13 esophageal carcinoma cells, and PSK             inhibited proliferation and induced apoptosis in these cells in a dose-dependent             manner. Based on these findings, the relationship between STAT3 and apoptosis             in these cells was investigated. Results showed that PSK inhibited the expression             of activated STAT3 and stimulated the expression of pro-apoptotic Bax in a dose-dependent             manner, without affecting the expression of anti-apoptotic Bcl-xL and Mcl-1. These             results indicate that PSK may induce apoptosis in esophageal carcinoma cells by             inhibiting the expression of activated STAT3.
authors.affiliation: Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural                     University of Medicine, Kyoto 602-8566, Japan.
authors.forename: Seiji
authors.initials: S
authors.lastname: Umehara
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Fujiwara
authors.forename: Atsushi
authors.initials: A
authors.lastname: Shiozaki
authors.forename: Momoko
authors.initials: M
authors.lastname: Todo
authors.forename: Akinobu
authors.initials: A
authors.lastname: Furutani
authors.forename: Masayuki
authors.initials: M
authors.lastname: Yoneda
authors.forename: Atsushi
authors.initials: A
authors.lastname: Ikai
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Tada
authors.forename: Shuhei
authors.initials: S
authors.lastname: Komatsu
authors.forename: Daisuke
authors.initials: D
authors.lastname: Ichikawa
authors.forename: Kazuma
authors.initials: K
authors.lastname: Okamoto
authors.forename: Toshiya
authors.initials: T
authors.lastname: Ochiai
authors.forename: Yukihito
authors.initials: Y
authors.lastname: Kokuba
authors.forename: Eigo
authors.initials: E
authors.lastname: Otsuji
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D004938:Esophageal Neoplasms; D006801:Humans; D010766:Phosphorylation; D011499:Protein Processing, Post-Translational / Q000187:drug effects; D011509:Proteoglycans / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D011509:Proteoglycans; D019253:Proto-Oncogene Proteins c-bcl-2; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; C010770:polysaccharide-K