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.

幽门螺杆菌可能通过萎缩性胃炎和肠化生间接诱发胃癌，也可能通过病原体引起的细胞增殖和抗凋亡直接诱发胃癌。在本研究中，我们在分子生物学水平上研究了（1）CagA 在细胞内信号转导激活中发挥的作用和（2）幽门螺杆菌对细胞凋亡的抑制，并揭示了 cagPAI 和 CagA 在每种现象中的作用。日本最近开始了通过根除幽门螺杆菌预防胃癌的临床研究。然而，由于日本约有5000万人幽门螺杆菌呈阳性，从经济角度以及反流性食管炎恶化等并发症的角度来看，一刀切地根除幽门螺杆菌可能并不可行。如果我们能够区分那些胃癌高危人群，那么胃癌的预防可能会变得切实可行，这将有助于了解幽门螺杆菌诱导的细胞增殖和抗凋亡的机制。

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。

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。

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。