mir -596介导的口腔鳞状细胞癌中LGALS3BP下调的替代机制探讨

Hui Li
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引用次数: 0

摘要

MicroRNAs (miRNAs)是内源性小的非编码rna,通过结合转录本的3' -非翻译区(UTR)负调控基因表达。然而,最近的证据表明,miRNA也可以结合转录本中的开放阅读框(ORF)区域进行下调。另一方面,先前的报道表明,miR-596在口腔鳞状细胞癌(OSCC)细胞中通过直接结合LGALS3BP的3' UTR靶向LGALS3BP,具有抑瘤功能。然而,目前尚不清楚该miRNA是否可以结合LGALS3BP的ORF区域。在本研究中,虽然在LGALS3BP的ORF区域中包含了四个推测的miR-596结合位点,但发现miR-596不能与这些位点结合。相反,结果表明LGALS3BP的表达可能在蛋白质水平上部分受到蛋白酶体系统的负调控。因此,这些发现可能有助于阐明miR-596在OSCC细胞中下调LGALS3BP抑制肿瘤作用的分子机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Exploration of Alternative Mechanism for MiR-596-mediated Down-regulation of LGALS3BP in Oral Squamous Cell Carcinoma.

MicroRNAs (miRNAs) are endogenous small non-coding RNAs that negatively regulate gene expression via binding to the 3' -untranslated region (UTR) of transcripts. However, recent evidence suggests that miRNA can also bind to the open reading frame (ORF) region within transcripts for its down-regulation. On the other hand, a previous report demonstrated that miR-596 has a tumor suppressor function by targeting LGALS3BP via directly binding to its 3' UTR in oral squamous cell carcinoma (OSCC) cells. However, it is not clear whether this miRNA can bind to the ORF region of LGALS3BP. In this study, although four putative binding sites of miR-596 were included within the ORF region of LGALS3BP, it was found that miR-596 could not bind to those sites. Instead, the results showed that the expression of LGALS3BP might be in part negatively regulated by the proteasome system at the protein level. Thus, these findings may help clarify the molecular mechanism of the tumor-suppressive effect through down-regulation of LGALS3BP by miR-596 in OSCC cells.

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