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在实验性大鼠模型中，miR-374介导胃癌相关间充质干细胞的恶性转化。

miR-374 mediates the malignant transformation of gastric cancer-associated mesenchymal stem cells in an experimental rat model.

作者信息

Ji Runbi, Zhang Xu, Qian Hui, Gu Hongbing, Sun Zixun, Mao Fei, Yan Yongmin, Chen Jingyan, Liang Zhaofeng, Xu Wenrong

机构信息

Department of Clinical Laboratory Medicine, The Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu 212002, P.R. China.

Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, P.R. China.

出版信息

Oncol Rep. 2017 Sep;38(3):1473-1481. doi: 10.3892/or.2017.5831. Epub 2017 Jul 18.

DOI:10.3892/or.2017.5831
PMID:28731132
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5549036/
Abstract

Mesenchymal stem cells (MSCs) are a critical component of the tumor microenvironment. Upon distinct pathological stimulus, MSCs show phenotypic and functional changes. Gastric cancer is one of the leading causes of cancer‑related deaths worldwide. The roles and mechanisms of MSCs in gastric cancer have not been well characterized. In the present study, we investigated the roles of MSCs in the malignant transformation from gastritis to gastric cancer using an N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastric cancer model. We isolated MSCs from the gastric tissues of normal (RGN-MSCs) and MNNG-exposed rats (RGI-MSCs), and compared the biological properties of RGI-MSCs with RGN-MSCs. We found that RGI-MSCs had increased proliferative and migratory capabilities than these capacities noted in the RGN-MSCs. In addition, RGI-MSCs produced higher levels of IL-6, CXCL10 and MCP-1 than RGN-MSCs. Moreover, RGI-MSCs promoted the migration of normal gastric mucosa epithelial cells by inducing epithelial-mesenchymal transition (EMT). The upregulation of miR-374 in RGI-MSCs was partially responsible for their increased proliferative and migratory capabilities. Collectively, our findings provide new evidence for the roles of MSCs in gastric carcinogenesis, suggesting that targeting gastric cancer-associated MSCs may represent a novel avenue for gastric cancer therapy.

摘要

间充质干细胞（MSCs）是肿瘤微环境的关键组成部分。在不同的病理刺激下，MSCs会表现出表型和功能变化。胃癌是全球癌症相关死亡的主要原因之一。MSCs在胃癌中的作用和机制尚未得到充分阐明。在本研究中，我们使用N-甲基-N'-硝基-N-亚硝基胍（MNNG）诱导的胃癌模型，研究了MSCs在从胃炎到胃癌的恶性转化中的作用。我们从正常大鼠（RGN-MSCs）和MNNG处理大鼠的胃组织中分离出MSCs，并比较了RGI-MSCs与RGN-MSCs的生物学特性。我们发现，RGI-MSCs比RGN-MSCs具有更强的增殖和迁移能力。此外，RGI-MSCs产生的IL-6、CXCL10和MCP-1水平高于RGN-MSCs。而且，RGI-MSCs通过诱导上皮-间质转化（EMT）促进正常胃黏膜上皮细胞的迁移。RGI-MSCs中miR-374 的上调部分解释了其增殖和迁移能力的增强。总体而言，我们的研究结果为MSCs在胃癌发生中的作用提供了新证据，表明靶向与胃癌相关的MSCs可能代表一种新的胃癌治疗途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/4f9e5b2c8fe5/OR-38-03-1473-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/7dc5664e936c/OR-38-03-1473-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/39581cbcc869/OR-38-03-1473-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/0468c078b1a8/OR-38-03-1473-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/40fcbff20c35/OR-38-03-1473-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/74c9eee1290f/OR-38-03-1473-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/4f9e5b2c8fe5/OR-38-03-1473-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/7dc5664e936c/OR-38-03-1473-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/39581cbcc869/OR-38-03-1473-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/0468c078b1a8/OR-38-03-1473-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/40fcbff20c35/OR-38-03-1473-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/74c9eee1290f/OR-38-03-1473-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b102/5549036/4f9e5b2c8fe5/OR-38-03-1473-g05.jpg

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