Elucidation of the mechanism of Epithelial-Mesenchymal Transition in peritoneal environment of gastric cancer

胃癌腹膜环境上皮-间质转化机制的阐明

• 批准号: 24791402
• 负责人: KINOSHITA Jun
• 金额: $ 1.83万
• 依托单位: Kanazawa University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24791402/
• 关键词: 胃癌; 腹膜播種; 上皮間葉転換; 腹膜中皮細胞; PSK; EMT; 線維化; HPMC

In this study, we evaluated the mechanism of EMT of Human PeritonealMesothelial Cell(HPMC) in in peritoneal environment of gastric cancer. We also investigated the inhibitory effect of PSK on the TGF/Smad signalling pathway and TGFb induced EMT in human HPMCs and gastric cancer cells. In vitro, TGFb increased the expression of E cadherin and decreased the expression of mesenchymal markers in HPMCs and which was suppressed by PSK. PSK suppressed TGFb induced phosphorylation of Smad2 in HPMCs in western blot analysis.In mouse subctaneous xenograft models, PSK inhibited the tumor fibrosis induced by co-inoculation of gastric cancer cells and HPMCs. PSK might have the potential to reduce TGFb induced activation of HPMCs in the peritoneal microenvironment of gastric cancer.

在这项研究中，我们评估了胃癌腹膜环境中人腹膜细胞（HPMC）EMT的机理。我们还研究了PSK对人HPMC和胃癌细胞中TGF/SMAD信号通路和TGFB诱导的EMT的抑制作用。在体外，TGFB增加了E钙粘着蛋白的表达，并降低了HPMC中间充质标记的表达，并被PSK抑制。 PSK抑制了TGFB在蛋白质印迹分析中诱导HPMC中SMAD2的磷酸化。在小鼠下异种移植模型中，PSK抑制了胃癌细胞和HPMC的共接种诱导的肿瘤纤维化。 PSK可能有可能减少TGFB诱导的HPMC激活在胃癌的腹膜微环境中。

项目成果

Effects of PSK on TGF-β induced epithelial to mesenchymal transition in peritoneal microenvironment of gastric cancer.

PSK对TGF-β诱导的胃癌腹膜微环境上皮间质转化的影响。

• 作者: 藤井千文;松村富穂;伊藤賢祐;肥田重明;谷口俊一郎;木下 淳
• 通讯作者: 木下 淳

Effects on TGF-β induced epithelial to mesenchymal transition in peritoneal microenvironment of gastric cancer

TGF-β诱导胃癌腹膜微环境上皮间质转化的影响

• 发表时间: 2013
• 作者: 木下 淳 伏田 幸夫 太田 哲生;他
• 通讯作者: 他