Promoting progression and clinicopathological significance of NEAT1 over-expression in bladder cancer

Abstract

Bladder cancer was the most important reason of cancer-related death around the world, and urgently requires new therapeutic methods targeting the malignant tumor. There are many reports that the long noncoding RNAs are participated in different cancers, however, limited data are found between the long noncoding RNAs and bladder cancer. Previous studies have indicated that lncRNAs play vital roles in gene regulatory processes which could influence carcinoma progression.It is well known that lncRNAs can't code proteins, however, controlling transcription was found in the life process.In the current study,we firstly reported that NEAT1 was consistently up-regulated in bladder cancer tissues compared to the matched tissues and bladder cancer cell lines compared to the normal bladder epithelial cell and the expression level of the NEAT1 in bladder cancer tissues is closely related to its clinical pathologic grade and TNM phase. Cell proliferation inhibition, cell migration suppression and apoptosis induction were detected by knockdown NEAT1. However, it is imperative that this hypothesis is further tested through. In conclusion, NEAT1 may play oncogenic roles and can be used as a therapeutic target for treating human bladder cancer. Our finding provides a new insight into the role of the LncRNA NEAT1 in the bladder cancer.

Long Noncoding RNA NEAT1, Regulated by the EGFR Pathway, Contributes to Glioblastoma Progression Through the WNT/β-Catenin Pathway by Scaffolding EZH2

“…NEAT1 can also be induced by poly I:C triggered by the toll-like receptor3-p38 pathway after infection with virus (13). Previous studies have shown that NEAT1 is an oncogene in various cancers, such as urinary bladder cancer, colorectal cancer, and nasopharyngeal carcinoma (14)(15)(16)(17). In addition to lncRNA, many tumor pathways have been shown to play an important role in glioma progression and invasion.…”

Functional dissection of NEAT1 using genome editing reveals substantial localization of the NEAT1_1 isoform outside paraspeckles

“…Unsurprisingly, there is also a strong link between high NEAT1 expression and more aggressive forms of cancer (Chakravarty et al 2014;Chai et al 2016;Chen et al 2016;Fu et al 2016;Ma et al 2016;Sun et al 2016;Wang et al 2016). In neurological systems, up-regulated expression of NEAT1 has also been observed in the early phase of amyotrophic lateral sclerosis and Huntington's disease, and more interestingly, its expression could also be acutely down-regulated in response to neuronal activity (Nishimoto et al 2013;Sunwoo et al 2016;Barry et al 2017).…”

“…The shorter NEAT1_1 isoform, albeit highly abundant, is not sufficient for paraspeckle formation and its involvement with the function of paraspeckles is still unclear (Mao et al 2011). Moreover, several functional studies reported that overexpression of NEAT1_1 may promote tumor growth and metastasis (Chakravarty et al 2014;Chen et al 2016;Sun et al 2016), and other studies in different cancer subtypes have indicated that high NEAT1_2 expression is linked to worse cancer prognosis via the activation of ATR (ataxia telangiectasia and Rad3-related) pathways (Adriaens et al 2016). These reports seem to imply that the two NEAT1 isoforms may be functionally distinct, or even opposite, entities, thus rendering the relationship between the two NEAT1 isoforms and paraspeckles enigmatic.…”

Long noncoding RNA NEAT1 suppresses hepatocyte proliferation in fulminant hepatic failure through increased recruitment of EZH2 to the LATS2 promoter region and promotion of H3K27me3 methylation

“…The lncRNA nuclearenriched abundant transcript 1 (NEAT1) was detected in primary hepatocytes isolated from fibrotic livers and identified as a regulator in the progression of liver fibrosis 7 . Moreover, previous studies have highlighted the role of lncRNA NEAT1 as an oncogene in bladder cancer, colorectal cancer, and hepatocellular carcinoma [8][9][10] . In addition, lncRNA NEAT1 can bind to enhancer of zeste homolog 2 (EZH2) and regulate the trimethylation of H3K27 in gene promoters in glioblastoma 11 .…”