Moradi Sadegh Lotfalah, Eslami Gita, Goudarzi Hossein, Hajishafieeha Zahra, Soleimani Masoud, Mohammadzadeh Adel, Ardeshirylajimi Abdolreza
Department of Microbiology, School of Medicine, International Branch, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, P.O. Box 19857-17443, Tehran, Iran.
Tumour Biol. 2016 Mar;37(3):3371-8. doi: 10.1007/s13277-015-4137-0. Epub 2015 Oct 7.
Recent studies have shown that Helicobacter pylori has a special role in tropism of mesenchymal stem cells (MSCs) towards gastric tissues. This study aimed to find the effects of H. pylori on human adipose-derived mesenchymal stem cells (hA-MSCs) transforming toward cancer cells and also metastasis of tumor cells by synergic effects of H. pylori and gastric epithelial cells (AGS) on MSCs. The expressions of p53, bcl-2, MMP-2, and MMP-9 were examined in hA-MSCs by qRT-PCR technique. Our results demonstrated that H. pylori tries to improve the hA-MSCs carcinogenic activities by overexpression of bcl2 gene as an anti-apoptosis agent against the p53 gene expression as main apoptosis agent. In addition, it showed that H. pylori effects in metastatic activities of hA-MSCs by upregulation of related genes in this process. Perhaps, when hA-MSCs are attracted toward H. pylori chronic or ulcer infected tissues for their tissue healing function, they will be trapped under special gastric microenvironment. We demonstrated the direct and synergic effects of H. pylori in hA-MSCs through alteration of related genes involved in carcinogenesis processes. Hence, understanding of H. pylori-induced molecular pathogenesis could be a powerful strategy not only in identifying the origin and initiation of gastric cancer but also in the treatment of related disease and modification of stem cell therapy methods in the future.
最近的研究表明,幽门螺杆菌在间充质干细胞(MSCs)向胃组织的归巢过程中具有特殊作用。本研究旨在探讨幽门螺杆菌对人脂肪来源的间充质干细胞(hA-MSCs)向癌细胞转化的影响,以及幽门螺杆菌与胃上皮细胞(AGS)对MSCs的协同作用对肿瘤细胞转移的影响。采用qRT-PCR技术检测hA-MSCs中p53、bcl-2、MMP-2和MMP-9的表达。我们的结果表明,幽门螺杆菌试图通过过表达作为抗凋亡因子的bcl2基因来对抗作为主要凋亡因子的p53基因表达,从而提高hA-MSCs的致癌活性。此外,研究表明幽门螺杆菌通过上调这一过程中的相关基因来影响hA-MSCs的转移活性。也许,当hA-MSCs因其组织修复功能被吸引到幽门螺杆菌慢性感染或溃疡感染的组织时,它们会被困在特殊的胃微环境中。我们通过改变参与致癌过程的相关基因,证明了幽门螺杆菌对hA-MSCs的直接和协同作用。因此,了解幽门螺杆菌诱导的分子发病机制不仅可能是识别胃癌起源和起始的有力策略,而且对未来相关疾病的治疗和干细胞治疗方法的改进也具有重要意义。