Mechanism of inflammation-associated gastro-intestinal carcinogenesis

炎症相关胃肠癌发生机制

• 批准号: 19390205
• 负责人: MAEDA Shin
• 金额: $ 11.81万
• 依托单位: Yokohama City University (2009-2010)The Institute for Adult Diseases, Asahi Life Foundation (2007-2008)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2007
• 资助国家: 日本
• 起止时间: 2007 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19390205/
• 关键词: 癌・動物; 癌; 炎症; NF-κB; 発がん; 消化管; 動物モデル; JNK

NF-kB/IKK and JNK pathways are important cell signaling pathways that regulate the gene cluster associated with the inflammation, apoptosis, and cell proliferation. Therefore it is suggested that these pathways play important roles of the development or progression of carcinomas. We used the mouse models and examined those functions in the gastrointestinal cancers. Cancer development was inhibited in the knockout mouse of NF-kB/IKK and JNK in the stomach cancer model. In addition, the inflammation-associated cancer of colon was inhibited by the IKK inhibitor. In summary, NF-kB/IKK and JNK were should be important for the generation or progression of gastrointestinal cancers and will become the treatment targets.

NF-kB/IKK和JNK通路是重要的细胞信号通路，调节与炎症、凋亡和细胞增殖相关的基因簇。提示这些通路在肿瘤的发生、发展中起重要作用。我们使用小鼠模型，并在胃肠道癌症中检查这些功能。在胃癌模型中，NF-kB/IKK和JNK基因敲除小鼠的肿瘤发展受到抑制。此外，IKK抑制剂对炎症相关性结肠癌有抑制作用。综上所述，NF-kB/IKK和JNK在胃肠道肿瘤的发生、发展中起重要作用，有望成为治疗的靶点。

项目成果

Omata M Requirement for IKKB in a Mouse Model of Pancreatic Ductal Adenocarcinoma

胰管腺癌小鼠模型中 IKKB 的 Omata M 需求

• 发表时间: 2010
• 作者: Sakamoto K;Okamoto M Nakagawa H;Hirata Y;Hayakawa Y;Nakata W;Ijichi H
• 通讯作者: Ijichi H

Deletion of ASK1 attenuates acetaminophen-induced liver injury by inhibiting JNK activation

ASK1 缺失通过抑制 JNK 激活减轻对乙酰氨基酚诱导的肝损伤

• 发表时间: 2008
• 期刊: Gastroenterology 135
• 作者: Nakagawa H;Maeda S;Hikiba Y;Ohmae T;Shibata W;Yanai A;Sakamoto K;Ogura K;Noguchi T;Karin M;Ichijo H;Omata M.
• 通讯作者: Omata M.

c-Jun NH2-terminal kinase 1 is a criticalregulator for the development of chemical-induced gastric cancer in mice.

c-Jun NH2 末端激酶 1 是化学诱导小鼠胃癌发生的关键调节因子。

• 发表时间: 2008
• 作者: Maeda S;Shibata W;Hikiba Y;Yanai A;Sakamotol K;Nakagawa H;Ogura K;Karin M;Omata M.
• 通讯作者: Omata M.

消化管癌発生、増殖におけるC-Jun N-terminal kinaseの役割

C-Jun N 末端激酶在胃肠癌发生和增殖中的作用

• 发表时间: 2007
• 作者: 前田 愼;芝 田渉;小俣 政男
• 通讯作者: 小俣 政男

Masao Omata Colon cancer-derived factors activate NF-κB in myeloid cells via TLR2 to link inflammation and tumorigenesis

Masao Omata 结肠癌衍生因子通过 TLR2 激活骨髓细胞中的 NF-κB，将炎症与肿瘤发生联系起来

• 发表时间: 2009
• 作者: Shin Maeda;Yohko Hikiba;Kei Sakamoto;Hayato Nakagawa;Yoku Hayakawa;Yoshihiro Hirata;Keiji Ogura
• 通讯作者: Keiji Ogura