miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells.
miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells.
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miR-320b 通过靶向人结直肠癌细胞中的 c-Myc 抑制细胞增殖
DOI：
10.1186/s12885-015-1728-5
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发表时间：
2015-10-20
期刊：
影响因子：
3.8
通讯作者：
Fu CG
中科院分区：
文献类型：
--
作者：
Wang H;Cao F;Li X;Miao H;E J;Xing J;Fu CG
MicroRNAs(MiRNAs)是一种小的非编码RNA，在肿瘤的发生过程中发挥着重要的作用。越来越多的证据表明，一种特定的miRNA：miR-320B在许多人类癌症中表达下调，包括结直肠癌(CRC)；这使得miR-320B可能在肿瘤发生中发挥关键作用的假设变得可信。然而，它在癌症发生中的作用仍然不清楚。本研究的目的是更好地阐明miR-320B在大肠癌生长中的作用。方法采用定量逆转录聚合酶链式反应(qRT-PCR)检测miR-320B在结直肠癌组织和5种结直肠癌细胞系中的表达。通过体内外实验分析miR-320B对细胞增殖的影响。此外，还进行了荧光素酶报告实验，以测量miR-320B的靶效应。最后，用qRT-PCR检测该基因在结直肠癌细胞系和组织中的信使RNA(MRNA)和蛋白水平，并通过Western印迹和免疫组织化学(IHC)染色进行验证。在结直肠癌细胞中miR-320B的过表达与细胞的体内外生长减少有统计学意义，而c-myc被认为是结直肠癌中miR-320B的靶基因。此外，c-Myc的上调可以减弱miR-320b的作用。结论我们将c-myc基因定位为miR-320B的靶基因，为进一步了解结直肠癌增殖的病理生理机制提供了新的思路，为治疗结直肠癌提供了新的治疗靶点。
BackgroundMicroRNAs (miRNAs) are small noncoding RNAs that potentially play a critical role in tumorigenesis. Mounting evidence indicates that one specific miRNA: miR-320b is down regulated in numerous human cancers, including colorectal cancer (CRC); making the hypothesis that miR-320b may play a key role in tumorigenesis plausible. However, its role in carcinogenesis remains poorly defined. The goal of this study is to better clarify the role of miR-320b in tumor growth of CRC.MethodsQuantitative reverse-transcription polymerase chain reaction (qRT-PCR) was conducted to detect the expression of miR-320b in CRC tissues and 5 CRC cell lines. The effect of miR-320b on cell proliferation was analyzedin vitroandin vivo. Furthermore, a luciferase reporter assay was performed to measure the target effects of miR-320b. Lastly, the messenger RNA (mRNA) and protein levels of the genec-MYCwere measured in CRC cell lines and tissues by qRT-PCR, and confirmed via Western blot and Immunohistochemical (IHC) staining.ResultsThe results presented here showed that miR-320b expression was down regulated in both CRC tissues and cells. Overexpression of miR-320b in CRC cells was statistically correlated with a decrease of cell growthin vitroandin vivo, whilec-MYCwas identified as a target gene of miR-320b in CRC. Furthermore, it was found that up-regulation of c-Myc can attenuate the effects induced by miR-320b.ConclusionsOur identification ofc-MYCas a target gene of miR-320b provides new insights into the pathophysiology of CRC proliferation, and identifies miR-320b as a novel therapeutic target for the treatment of CRC.