NCYM facilitates cell proliferation and invasion in Wilms tumor by regulating SIX1/β-catenin axis

NCYM通过调控SIX1/β-catenin轴促进Wilms肿瘤细胞的增殖和侵袭。

阅读:2

Abstract

Recently, accumulating studies demonstrate that some long non-coding RNAs (lncRNAs) contain open read frames and have protein/peptide-coding potential. NCYM is a 109-amino acid product encoded by lncRNA MYCNOS variant 2 that is an antisense transcript of MYCN oncogene. NCYM is amplified in human neuroblastomas and associated with poor prognosis. However, its functional role in Wilms tumor (WT) remains unclear. In this study, we identified lncRNA MYCNOS as a promising prognostic factor in Wilms tumor through bioinformatics analysis. The expression of NCYM and downstream genes was determined by western blotting. Cell proliferation, migration, and invasion were measured by CCK-8, wound healing and Transwell assays, respectively. Cell apoptosis was evaluated by flow cytometry assay. The subcutaneous xenograft and lung metastasis mouse model were established by the armpit injection or tail intravenous injection of WT cells, respectively. Our results showed that NCYM was validated to be abundantly expressed in Wilms tumor cell lines and tissues. The exogenous overexpression of NCYM promoted WT cell proliferation, migration, and invasion. The silencing of SIX1 expression abolished the pro-growth effect of NCYM and downregulated β-catenin in WT. Additionally, NCYM facilitated tumor growth and formation of lung metastasis in vivo. In summary, the exogenous overexpression of NCYM could play a critical role in WT progression by mediating SIX1 and β-catenin as an oncopromoting factor.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。