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Long non-coding RNA Linc00675 suppresses cell proliferation and metastasis in colorectal cancer via acting on miR-942 and Wnt/beta-catenin signaling

机译:长期非编码RNA LINC00675通过作用于MIR-942和WNT / Beta-catenin信号传导抑制细胞增殖和转移

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Substantial evidence has demonstrated the involvement of long non-coding RNAs (lncRNAs) in the development and progression of colorectal cancer (CRC) via their regulation on cancer cell proliferation, apoptosis, invasion and metastasis pathways. The current study aimed to understand the role of lncRNA Linc00675 in the progression and metastasis of CRC and to identify the potential lncRNA-miRNA interactions and signaling pathways underlying the mechanisms of action of Linc00675 in CRC. Our data firstly demonstrated the down-regulation of Linc00675 in both CRC cells and clinical CRC tissues. Expression of Linc00675 was also relatively low in metastatic tumors and advanced tumors. Further studies also showed that overexpression of Linc00675 inhibited the proliferation, invasion and migration of CRC cells. In addition, our data also revealed the negative regulation of miR-942 by Linc00675 and the relatively higher expression of miR-942 in clinical CRC tissues. More importantly, the inhibitory effect of Linc00675 on proliferation, invasion and migration of HCT116 cells was also significantly attenuated in the presence of miR-942 mimic, suggesting that down-regulation of miR-942 represented one of the mechanisms by which Linc00675 inhibited the proliferation and metastasis of CRC. Furthermore, we also demonstrated the inhibition of Wnt/beta-catenin signaling in the Linc00675/miR-942 regulated pathway in CRC cells. Taken together, our findings suggested Linc00675 as a potential molecular marker and target for the diagnosis and treatment of CRC and enhanced the current understanding on the mechanisms of action of Linc00675 in CRC.
机译:实质性证据证明,通过调节癌细胞增殖,细胞凋亡,侵袭和转移途径的调节,展示了长期非编码RNA(LNCRNA)在结肠直肠癌(CRC)的开发和进展中的参与。目前的研究旨在了解LNCRNA LINC00675在CRC的进展和转移中的作用,并鉴定CRC中LINC00675的作用机制的潜在的LNCRNA-miRNA相互作用和信号通路。我们的数据首先展示了在CRC细胞和临床CRC组织中的LINC00675的下调。 LINC00675的表达在转移性肿瘤和晚期肿瘤中也相对较低。进一步的研究还表明,LINC00675的过度表达抑制了CRC细胞的增殖,侵袭和迁移。此外,我们的数据还揭示了LINC00675的miR-942的负调节以及临床CRC组织中miR-942的相对较高的表达。更重要的是,在MiR-942模拟的情况下,LINC00675对HCT116细胞增殖,侵袭和迁移的抑制作用也显着衰减,表明MiR-942的下调代表了LINC00675抑制增殖的机制之一和crc的转移。此外,我们还证明了在CRC细胞中LINC00675 / miR-942调节途径中Wnt /β-catenin信号传导的抑制。我们的研究结果表明,LINC00675作为潜在的分子标记和诊断和治疗CRC的目标,并加强了目前关于CRC在CRC中LINC00675的作用机制的理解。

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