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首页> 外文期刊>Frontiers in Cell and Developmental Biology >Cancer-Preventive Role of Bone Marrow-Derived Mesenchymal Stem Cells on Colitis-Associated Colorectal Cancer: Roles of Gut Microbiota Involved
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Cancer-Preventive Role of Bone Marrow-Derived Mesenchymal Stem Cells on Colitis-Associated Colorectal Cancer: Roles of Gut Microbiota Involved

机译：骨髓衍生的间充质干细胞对结肠炎相关结直肠癌的癌症 - 预防作用：肠道微生物症涉及的作用

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Background: Mesenchymal stem cells (MSCs) are widely studied in inflammatory bowel disease (IBD) in preclinical rodent model and clinical patients. However, previous studies have produced controversial results regarding whether MSCs promote or inhibit tumor development. This study aims to evaluate the role of bone marrow-derived MSCs and the potential mechanism in colitis-associated colon cancer model (CAC). Methods: MSCs were isolated from bone marrow of GFP-transgenic mice and identified by flow cytometry. CAC mice model was induced by azoxymethane (AOM) and dextran sulfate sodium (DSS) and MSCs were injected intraperitoneally (i.p.) once per week. Weight loss, colon length, tumor number and average tumor size were assessed macroscopically. MSCs localization was detected by immunofluorescence staining, tumor cell proliferation and apoptosis were measured by immunohistochemistry staining of Ki-67 and TUNEL assay, respectively. The colonic tumor tissues were isolated for RNA-seq and fecal samples were collected for 16s rRNA sequencing of microbiome. Results: After injection intraperitoneally, MSCs could migrate to colon and suppress initiation of colitis-related neoplasm. This tumor suppressive effect was characterized by less weight loss, longer colon length and decreased tumor numbers. Moreover, MSCs decreased tumor cell proliferation and increased tumor cell apoptosis. Furthermore, MSCs could inhibit chronic inflammation assessed by RNA-sequencing and promote gut microbiome normalization detected by 16S rRNA sequencing. Conclusion: The results proven that MSCs could migrate to colon, inhibit chronic inflammation and regulate gut microbiome dysbiosis so as to suppress the development of CAC.
机译：背景：间充质干细胞（MSCs）广泛研究临床前啮齿动物模型和临床患者的炎性肠病（IBD）。然而，先前的研究已经产生了有关MSCs促进或抑制肿瘤发育的争议结果。本研究旨在评估骨髓衍生的MSCs的作用和结肠炎相关的结肠癌模型（CAC）的潜在机制。方法：从GFP-转基因小鼠的骨髓中分离MSC，并通过流式细胞术鉴定。 CAC小鼠模型由偶氮甲烷（AOM）诱导，硫酸硫酸钠（DSS）和MSC每周腹膜内（I.P.）注射一次。在宏观上评估体重减轻，结肠长度，肿瘤数和平均肿瘤大小。通过免疫荧光染色检测MSCs定位，通过分别通过免疫组织化学染色和TUNEL测定法测量肿瘤细胞增殖和细胞凋亡。将结肠肿瘤组织分离用于RNA-SEQ，并收集粪便样品进行16S rRNA测序微生物组。结果：腹膜内注射后，MSCs可以迁移到结肠癌和抑制与结肠炎相关肿瘤的引发。这种肿瘤抑制效果的特征在于减肥，结肠长度更长，肿瘤数减少。此外，MSCs降低肿瘤细胞增殖和增加的肿瘤细胞凋亡。此外，MSCs可以抑制通过RNA测序评估的慢性炎症，并促进通过16S rRNA测序检测的肠道微生物组归一化。结论：结果证明，MSCs可以迁移到结肠，抑制慢性炎症和调节肠道微生物脱菌病，以抑制CAC的发育。

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