Molecular Biological Studies on Cellular Proliferation and Apoptosis Induced by H. pylori

幽门螺杆菌诱导细胞增殖和凋亡的分子生物学研究

• 批准号: 14570445
• 负责人: YOSHIDA Haruhiko
• 金额: $ 2.24万
• 依托单位: THE UNIVERSITY OF TOKYO
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2002
• 资助国家: 日本
• 起止时间: 2002 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14570445/
• 关键词: Helicobacter pylori; Cellular Proliferation; Anti-Apoptosis; Apoptosis; Serum Responsive Element; c-IAP2; Carcinogenesis; NFκB; 細胞内信号伝達; CagA; スナネズミ

Gastric carcinogenesis may be induced by H. pylori indirectly through atrophic gastritis and intestinal metaplasia and directly through cellular proliferation and anti-apoptosis caused by the pathogen. We investigated in this study (1) the role played by CagA in the activation of intracellular signal transduction and (2) the suppression of apoptosis by H. pylori on molecular biological levels and revealed the role of cagPAI and CagA in each phenomenon. Clinical studies on the prevention of stomach cancer by H. pylori eradication has recently been started in Japan. However, since there are about 50 million people positive for H. pylori in Japan, indiscriminate eradication may not be feasible from the economic viewpoint and also concerning complications such as exacerbation of regurgitation esophagitis. Prevention of stomach cancer may become practical if we can discriminate those who are at a high risk for stomach cancer, which will be facilitated by the understanding of mechanisms underlying cellular proliferation and anti-apoptosis induced by H. pylori.

幽门螺杆菌可通过萎缩性胃炎和肠化生间接诱导胃癌发生，也可通过病原菌引起的细胞增殖和抗凋亡直接诱导胃癌发生。本研究从分子生物学水平探讨了(1)CagA对细胞内信号转导的激活作用和(2)幽门螺杆菌对细胞凋亡的抑制作用，揭示了cagPAI和CagA在这两种现象中的作用。通过根除幽门螺杆菌预防胃癌的临床研究最近在日本开始。然而，由于日本约有5000万人感染幽门螺杆菌，从经济角度和反流性食管炎加剧等并发症来看，不分青红皂白地根除幽门螺杆菌可能并不可行。如果我们能够区分胃癌的高危人群，了解幽门螺杆菌诱导的细胞增殖和抗凋亡机制将有助于预防胃癌的发生。

项目成果

Maeda S, Mitsuno Y, Yoshida H, et al.: "Analysis of apoptotic and antiapoptotic signalling pathways induced by Helicobacter pylon."Gut. 50. 774-778 (2002)

Maeda S、Mitsuno Y、Yoshida H 等人：“幽门螺杆菌诱导的凋亡和抗凋亡信号通路分析”。

Yanai A, Hirata Y, Mitsuo Y, et al.: "Helicobacter pylori induces antiapoptosis through nuclear factor-kappaB activation"J Infectious Disease. 188. 1741-1751 (2003)

Yanai A、Hirata Y、Mitsuo Y 等人：“幽门螺杆菌通过核因子 kappaB 激活诱导抗凋亡”J 传染病。

Mitsuno Y, Yoshida H, et al.: "Helicobacter pylon activates the proto-oncogene c-fos through SRE transactivation."Biochemical and Biophysical Research Communications. 291. 868-874 (2002)

Mitsuno Y、Yoshida H 等人：“幽门螺杆菌通过 SRE 反式激活激活原癌基因 c-fos。”生物化学和生物物理研究通讯。

Maeda S, Yoshida H, Mitsuno Y, et al.: "Analysis of apoptotic and antiapoptotic signaling pathways induced by Helicobacter pylori"Gut. 50. 771-778 (2002)

Maeda S、Yoshida H、Mitsuno Y 等人：“幽门螺杆菌诱导的凋亡和抗凋亡信号通路分析”Gut。

Mitsuno Y, Maeda S, Yoshida H, et al.: "Helicobacter pylori activates the proto-oncogene c-fos through SRE transactivation"Biochem Bioohys Res Commun. 291. 868-874 (2002)

Mitsuno Y、Maeda S、Yoshida H 等人：“幽门螺杆菌通过 SRE 反式激活激活原癌基因 c-fos”Biochem Bioohys Res Commun。