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首页> 外文期刊>Molecular Cancer >miR-133b, a muscle-specific microRNA, is a novel prognostic marker that participates in the progression of human colorectal cancer via regulation of CXCR4 expression
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miR-133b, a muscle-specific microRNA, is a novel prognostic marker that participates in the progression of human colorectal cancer via regulation of CXCR4 expression

机译：miR-133b是一种肌肉特异性microRNA，是一种新型的预后指标，可通过调节CXCR4表达参与人类大肠癌的进展

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Background MicroRNA-133b (miR-133b), which is a muscle-specific microRNA, has been reported to be downregulated in human colorectal carcinoma (CRC) when compared to adjacent non-tumor tissue. However, its diagnostic value and role in CRC have yet to be described. CXC chemokine receptor-4 (CXCR4), which participates in multiple cell processes such as cell invasion-related signaling pathways, was predicted to be a potential target of miR-133b. The aim of this study was to investigate the associations and functions of miR-133b and CXCR4 in CRC initiation and invasion. Methods Mature miR-133b and CXCR4 expression levels were detected in 31 tumor samples and their adjacent, non-tumor tissues from patients with CRC, as well as in 6 CRC cell lines, using real-time quantitative RT-PCR (qRT-PCR). Luciferase reporter assays and Western blots were used to validate CXCR4 as a putative target gene of miR-133b. Regulation of CXCR4 expression by miR-133b was assessed using qRT-PCR and Western blot analysis, and the effects of exogenous miR-133b and CXCR4 on cell invasion and migration were evaluated in vitro using the SW-480 and SW-620 CRC cell lines. Results A significant downregulation of miR-133b was observed in 93.55% of CRC tissues, and the expression of miR-133b was much lower in metastatic tumors (stage C and D, stratified by the Modified Dukes Staging System) than in primary tumors (stage A and B). In contrast, CXCR4 protein expression significantly increased in 52.63% of CRC samples, and increased CXCR4 expression in CRC was associated with advanced tumor stage. CXCR4 was shown to be a direct target of miR-133b by luciferase reporter assays, and transfection of miR-133b mimics inhibited invasion and stimulated apoptosis of SW-480 and SW-620 CRC cells. Conclusions Our study demonstrated that downregulated miR-133b contributed to increased cell invasion and migration in CRC by negatively regulating CXCR4. These findings may be significant for the development of therapy target for CRC.
机译：背景技术据报道，与邻近的非肿瘤组织相比，人类特定结直肠癌（CRC）中的MicroRNA-133b（miR-133b）是一种肌肉特异性microRNA，其表达下调。但是，其在CRC中的诊断价值和作用尚待描述。 CXC趋化因子受体4（CXCR4）参与了多个细胞过程，例如与细胞入侵相关的信号传导途径，预计将成为miR-133b的潜在靶标。这项研究的目的是调查miR-133b和CXCR4在CRC起始和侵袭中的关联和功能。方法采用实时定量RT-PCR（qRT-PCR）方法检测31例CRC患者及其附近非肿瘤组织以及6种CRC细胞中成熟miR-133b和CXCR4的表达水平。 。荧光素酶报告基因测定和Western印迹用于验证CXCR4是miR-133b的假定靶基因。使用qRT-PCR和Western blot分析评估miR-133b对CXCR4表达的调节，并使用SW-480和SW-620 CRC细胞系在体外评估外源性miR-133b和CXCR4对细胞侵袭和迁移的影响。 。结果在93.55％的CRC组织中观察到miR-133b的显着下调，并且在转移性肿瘤（C和D期，经改良的Dukes分期系统分层）中，miR-133b的表达远低于原发性肿瘤（分期） A和B）。相反，在52.63％的CRC样本中CXCR4蛋白表达显着增加，并且在CRC中CXCR4表达增加与晚期肿瘤分期相关。 CXCR4被萤光素酶报告基因检测证明是miR-133b的直接靶标，miR-133b模拟物的转染抑制SW-480和SW-620 CRC细胞的侵袭并刺激其凋亡。结论我们的研究表明，miR-133b的下调通过负调控CXCR4促进了CRC细胞侵袭和迁移。这些发现对于开发CRC治疗靶标可能是重要的。

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