International Journal of Oncology 2012-07-01

PSK induces apoptosis through the inhibition of activated STAT3 in human esophageal carcinoma cells.

Seiji Umehara, Hitoshi Fujiwara, Atsushi Shiozaki, Momoko Todo, Akinobu Furutani, Masayuki Yoneda, Atsushi Ikai, Hiroyuki Tada, Shuhei Komatsu, Daisuke Ichikawa, Kazuma Okamoto, Toshiya Ochiai, Yukihito Kokuba, Eigo Otsuji

Index: Int. J. Oncol. 41(1) , 61-6, (2012)

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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.