Protein-bound polysaccharide decreases invasiveness and proliferation in pancreatic cancer by inhibition of hedgehog signaling and HIF-1¦Á pathways under hypoxia

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• 作者：Hideya Onishi^a ; ^{ohnishi@surg1.med.kyushu-u.ac.jp} ; Takafumi Morisaki^a ; Fumihiko Nakao^a ; Seiichi Odate^a ; Takashi Morisaki^b ; Mitsuo Katano^a
• 关键词：PSK ; protein-bound polysaccharide ; PDAC ; pancreatic ductal adenocarcinoma ; Hh ; hedgehog ; HIF ; hypoxia inducible factor ; Smo ; Smoothened ; MMP ; metalloproteinases
• 刊名：Cancer Letters
• 出版年：2013
• 出版时间：28 July, 2013
• 年：2013
• 卷：335
• 期：2
• 页码：289-298
• 全文大小：2100 K

文摘

To develop an effective therapeutic approach to pancreatic ductal adenocarcinoma (PDAC), we focused on the antitumor mechanism of protein-bound polysaccharide (PSK) under hypoxia. PSK decreased proliferation in PDAC cells under hypoxia but not normoxia. PSK also showed anti-tumor effects in vivo, inhibited invasiveness of PDAC cells, and decreased the expression of HIF-1¦Á and hedgehog (Hh) signaling-related molecules under hypoxia. Inhibition of HIF-1¦Á and Hh signaling reduced proliferation and invasiveness in PDAC cells under hypoxia. In conclusion, we found new PSK-related pathways in invasiveness and proliferation in PDAC under hypoxia. PSK may be a promising therapeutic drug to treat refractory PDAC.