幽门螺杆菌与H+-K+-ATP酶在胃癌发病中的研究进展
Research Advances of Helicobacter pylori and H+-K+-ATPase in the Pathogenesis of Gastric Cancer
DOI: 10.12677/ACM.2023.1361447, PDF,    科研立项经费支持
作者: 马秀雯：青海大学研究生院，青海 西宁 ；王学红*：青海大学附属医院消化内科，青海 西宁
关键词: 胃癌；幽门螺杆菌；H+-K+-ATP酶；Gastric Cancer； Helicobacter pylori； H+-K+-ATPase
摘要: 胃癌是上消化道最常见的恶性肿瘤之一，幽门螺杆菌(Helicobacter pylori, H. pylori)感染是其发病的主要危险因素，但是，幽门螺杆菌在胃癌发生过程中的具体机制仍未阐明。H+-K+-ATP酶在胃粘膜壁细胞保持正常结构、维持正常的胃内酸性环境中起着重要作用，当H+-K+-ATP酶表达过低会导致胃酸分泌减少，使胃粘膜发生萎缩，最终进展为癌症。幽门螺杆菌感染后可以改变H+-K+-ATP酶的表达，共同参与胃癌的发生发展。因此，本文对幽门螺杆菌感染与H+-K+-ATP酶在胃癌在胃癌发病机制中的作用作一综述。
Abstract: Gastric cancer is one of the most common malignant tumors in the upper digestive tract, and Heli-cobacter pylori (H. pylori) infection is the main risk factor. However, the specific mechanism of Heli-cobacter pylori in the development of gastric cancer remains unclear. H+-K+-ATPase plays an im-portant role in maintaining the normal structure of gastric mucosal parietal cells and maintaining the normal gastric acidic environment. When H+-K+-ATPase expression is too low, the gastric acid secretion will be reduced, and the gastric mucosa will atrophy and eventually progress to cancer. Helicobacter pylori infection can change the expression of H+-K+-ATPase and participate in the oc-currence and development of gastric cancer. Therefore, this paper reviews the role of Helicobacter pylori infection and H+-K+-ATPase in the pathogenesis of gastric cancer.
文章引用：马秀雯, 王学红. 幽门螺杆菌与H+-K+-ATP酶在胃癌发病中的研究进展[J]. 临床医学进展, 2023, 13(6): 10335-10339. https://doi.org/10.12677/ACM.2023.1361447

参考文献

[1] 刘宗超, 李哲轩, 张阳, 等. 2020全球癌症统计报告解读[J]. 肿瘤综合治疗电子杂志, 2021, 7(2): 1-14.
[2] 陈心足, 胡建昆, SIGES研究组. 胃癌防控策略的探索与优化: 流行病学、病原微生物及危险因素[J]. 中国普外基础与临床杂志, 2023, 30(1): 86-90.
[3] 邹艳花, 许可葵, 李灿, 等. 2019年湖南省肿瘤登记地区恶性肿瘤发病与死亡及2015-2019年变化趋势分析[J]. 中国肿瘤, 2023: 1-9.
[4] 张思维, 郑荣寿, 孙可欣, 等. 2016年中国恶性肿瘤分地区发病和死亡估计: 基于人群的肿瘤登记数据分析[J]. 中国肿瘤, 2023, 32(5): 321-332.
[5] 张琴, 谭婷婷, 王明婷, 等. 胃癌的病因及治疗研究进展[J]. 基层医学论坛, 2020, 24(7): 1008-1010.
[6] 简丹丹, 吴清明, 龙辉. 胃癌可控危险因素10年研究进展[J]. 临床消化病杂志, 2021, 33(5): 374-378.
[7] Yao, X. and Smolka, A.J. (2019) Gastric Parietal Cell Physiology and Helicobacter pylori-Induced Disease. Gastroenterology, 156, 2158-2173. [Google Scholar] [CrossRef] [PubMed]
[8] Dubey, V., Han, M., Kopec, W., et al. (2018) K+ Binding and Proton Redistribution in the E2P State of the H+, K+-ATPase. Scientific Reports, 8, Article No. 12732. [Google Scholar] [CrossRef] [PubMed]
[9] Smolka, A.J., Larsen, K.A., Schweinfest, C.W., et al. (1999) H,K-ATPase Alpha Subunit C-Terminal Membrane Topology: Epitope Tags in the Insect Cell Expression System. Bio-chemical Journal, 340, 601-611. [Google Scholar] [CrossRef] [PubMed]
[10] Lei, W.Y., Lee, J.Y., Chuang, S.L., et al. (2023) Eradicating Helicobacter pylori via 13C-Urea Breath Screening to Prevent Gastric Cancer in Indigenous Communities: A Population-Based Study and Development of a Family Index-Case Method. Gut. [Google Scholar] [CrossRef] [PubMed]
[11] Zhang, F., Chen, C., Hu, J., et al. (2019) Molecular Mechanism of Helicobacter pylori-Induced Autophagy in Gastric Cancer. On-cology Letters, 18, 6221-6227. [Google Scholar] [CrossRef] [PubMed]
[12] Shimizu, T., Chiba, T. and Marusawa, H. (2017) Helicobacter pylori-Mediated Genetic Instability and Gastric Carcinogenesis. Current Topics in Microbiology and Immunology, 400, 305-323. [Google Scholar] [CrossRef] [PubMed]
[13] He, J., Hu, W., Ouyang, Q., et al. (2022) Helicobacter pylori Infection Induces Stem Cell-Like Properties in Correa Cascade of Gastric Cancer. Cancer Letters, 542, Article ID: 215764. [Google Scholar] [CrossRef] [PubMed]
[14] Zheng, S.Y., Zhu, L., Wu, L.Y., et al. (2023) Helico-bacter pylori-Positive Chronic Atrophic Gastritis and Cellular Senescence. Helicobacter, 28, e12944. [Google Scholar] [CrossRef] [PubMed]
[15] Park, Y.H. and Kim, N. (2015) Review of Atrophic Gastritis and Intestinal Metaplasia as a Premalignant Lesion of Gastric Cancer. Journal of Cancer Prevention, 20, 25-40. [Google Scholar] [CrossRef] 
[16] 张鑫, 刘纯杰. 幽门螺杆菌感染引起的免疫应答与免疫逃逸机制研究进展[J]. 世界华人消化杂志, 2018, 26(31): 1832-1842.
[17] Gall, A., Gaudet, R.G., Gray-Owen, S.D., et al. (2017) TIFA Signaling in Gastric Epithelial Cells Initiates the Cag Type 4 Secretion System-Dependent Innate Immune Response to Helicobacter pylori Infection. mBio, 8, e01168-17. [Google Scholar] [CrossRef] 
[18] Cho, J.H., Jeon, S.R. and Jin, S.Y. (2020) Clinical Applicability of Gastroscopy with Narrow-Band Imaging for the Diagnosis of Helicobacter pylori Gastritis, Precancerous Gastric Lesion, and Neoplasia. World Journal of Clinical Cases, 8, 2902-2916. [Google Scholar] [CrossRef] [PubMed]
[19] Liu, W., Yang, L.J., Liu, Y.L., et al. (2020) Dynamic Characterization of Intestinal Metaplasia in the Gastric Corpus Mucosa of Atp4a-Deficient Mice. BioScientific Reports, 40, 28. [Google Scholar] [CrossRef] 
[20] Tapia, O., Riquelme, I., Leal, P., et al. (2014) The PI3K/AKT/mTOR Pathway Is Activated in Gastric Cancer with Potential Prog-nostic and Predictive Significance. Virchows Archiv, 465, 25-33. [Google Scholar] [CrossRef] [PubMed]
[21] Pan, Y., Wang, X., He, Y., et al. (2021) Tumor Suppressor ATP4B Serve as a Promising Biomarker for Worsening of Gastric Atrophy and Poor Differentiation. Gastric Cancer, 24, 314-326. [Google Scholar] [CrossRef] [PubMed]
[22] Dong, Z., Zhang, X., Chen, X., et al. (2019) Signifi-cance of Serological Gastric Biopsy in Different Gastric Mucosal Lesions: An Observational Study. Clinical Laboratory, 65, 2141-2148. [Google Scholar] [CrossRef] 
[23] Neu, B., Randlkofer, P., Neuhofer, M., et al. (2002) Helicobacter pylori Induces Apoptosis of Rat Gastric Parietal Cells. The American Journal of Physiolo-gy-Gastrointestinal and Liver Physiology, 283, G309-G318. [Google Scholar] [CrossRef] [PubMed]
[24] Beil, W., Birkholz, C., Wagner, S., et al. (1994) Interaction of Heli-cobacter pylori and Its Fatty Acids with Parietal Cells and Gastric H+/K+-ATPase. Gut, 35, 1176-1180. [Google Scholar] [CrossRef] [PubMed]
[25] Correa, P. (1992) Human Gastric Carcinogenesis: A Multistep and Mul-tifactorial Process—First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. Cancer Re-search, 52, 6735-6740.
[26] 朱怡臻, 贾西云, 徐倩, 等. E-cadherin、STMN1和ATP4B在胃癌细胞中表达的关系及意义[J]. 医药论坛杂志, 2022, 43(8): 11-16.
[27] Osawa, H., Kita, H., Ohnishi, H., et al. (2006) Helicobacter pylori Eradication Induces Marked Increase in H+/K+- Adenosine Triphosphatase Expression without Altering Parietal Cell Number in Human Gastric Mucosa. Gut, 55, 152-157. [Google Scholar] [CrossRef] [PubMed]
[28] Hsiung, H.Y., Fann, J.C., Yen, A.M., et al. (2016) Stage-Specific Dietary Factors Associated with the Correa Multistep and Multifacto-rial Process of Human Gastric Carcinogenesis. Nutrition and Cancer, 68, 598-610. [Google Scholar] [CrossRef] [PubMed]

为你推荐