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首页> 外文期刊>Journal of cellular physiology. >Long noncoding MAGI2-AS3 promotes colorectal cancer progression through regulating miR-3163/TMEM106B axis
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Long noncoding MAGI2-AS3 promotes colorectal cancer progression through regulating miR-3163/TMEM106B axis

机译：长非编码MAGI2-AS3促进结直肠通过调节癌症恶化mir - 3163 / TMEM106B轴

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Colorectal cancer (CRC), is mostly derived from normal colon epithelial cells, and has been reported to be one of most common gastrointestinal malignancies globally. An increasing number of researchers have claimed that long noncoding RNAs (IncRNAs) exert significant functions in tumor progression. Nevertheless, the function of MAGI2-AS3 remains uncertain in CRC. The expression of MAGI2-AS3, miR-3163, and transmembrane protein 106B (TMEM106B) messenger RNA was examined by quantitative real-time polymerase chain reaction. Cell apoptosis was measured by caspase-3 activity test. Cell proliferation was tested by cell-counting kit 8 and 5-ethynyl-2'-deoxyuridine assays. Cell migration was detected by transwell assay. Western blot analysis examined the protein expression of TMEM106B. The expression of Ki-67 was evaluated by immunohistochemistry assay. The binding capacity between miR-3163 and MAGI2-AS3 (or TMEM106B) was studied by radioimmunoprecipitation and luciferase reporter assays. The expression of MAGI2-AS3 and TMEM106B was conspicuously upregulated whereas miR-3163 presented lower expression in CRC cells. MAGI2-AS3 deficiency facilitated cell apoptosis but hampered cell proliferation and migration. MAGI2-AS3 combined with miR-3163 and negatively regulated miR-3163 expression. In addition, the administration of sh-MAGI2-AS3 or miR-3163 mimics suppressed CRC cell growth in vivo. Subsequently, miR-3163 targeted TMEM106B and the transfection of sh-MAGI2-AS3 or miR-3163 mimics downregulated TMEM106B expression. Rescue assays verified that TMEM106B overexpression recovered the effects of MAGI2-AS3 inhibition on cell apoptosis, proliferation, and migration in CRC. MAGI2-AS3 drives CRC progression through regulating miR-3163/TMEM106B axis. This supplies innovative insights on the investigation of molecular mechanism in CRC progression.
机译：结直肠癌(CRC),主要是来自正常结肠上皮细胞,一直最常见的一种全球胃肠道恶性肿瘤。越来越多的研究人员声称长非编码rna (IncRNAs)施加肿瘤恶化的重要功能。然而,MAGI2-AS3的功能仍然存在CRC的不确定。mir - 3163,跨膜蛋白106 b(TMEM106B)信使核糖核酸检测定量实时聚合酶链反应。细胞凋亡是衡量caspase-3活动测试。细胞计数设备8和5-ethynyl-2脱氧尿苷化验。化验。TMEM106B的表情。被免疫组织化学分析评估。mir - 3163和MAGI2-AS3之间的结合能力(或TMEM106B)进行了研究radioimmunoprecipitation和荧光素酶报告化验。是明显调节而mir - 3163提出了在CRC细胞低表达。MAGI2-AS3缺乏促进细胞凋亡但阻碍了细胞增殖和迁移。MAGI2-AS3结合mir - 3163和消极监管mir - 3163的表达。政府sh-MAGI2-AS3或mir - 3163模拟抑制CRC体内细胞生长。mir - 3163目标TMEM106B和转染sh-MAGI2-AS3或mir - 3163模仿表达下调TMEM106B表达式。TMEM106B超表达的影响中恢复过来MAGI2-AS3抑制细胞凋亡,增殖,在CRC和迁移。通过调节驱动CRC进展mir - 3163 / TMEM106B轴。在调查的分子的见解在CRC发展机制。

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