Nuclear-enriched abundant transcript 1 as a diagnostic and prognostic biomarker in colorectal cancer

Wu, Yuchen; Li, Yang; Zhao, Jiang; Li, Cong; Nie, Jia; Liu, Fangqi; Zhuo, Changhua; Zheng, Yaxin; Li, Bin; Wang, Zhimin; Xu, Ye

doi:10.1186/s12943-015-0455-5

Cited by 125 publications

(107 citation statements)

References 52 publications

Supporting

Mentioning

100

Contrasting

Order By: Relevance

“…Neat1/NEAT1 has been shown previously to control several aspects of cell behavior by enhancing or decreasing cell division, inhibiting cell death, and increasing migration (Chakravarty et al 2014;Chen et al 2015;Choudhry et al 2015;Wu et al 2015;Ma et al 2016;Wang et al 2016). Our findings in the pancreatic cancer model support the notion that Neat1 inhibits cell proliferation.…”

Section: Discussionsupporting

confidence: 86%

“…However, beyond the suggestion that NEAT1 is an oncogene, other studies have suggested that NEAT1 acts as a tumor suppressor in certain contexts. NEAT1 is down-regulated in some cancers relative to normal tissue, augmented NEAT1_2 levels were shown to predict better overall survival in colorectal cancer patients, and increased NEAT1 levels were associated with enhanced apoptosis in irradiated chronic lymphocytic leukemia cells (Gibb et al 2011;Blume et al 2015;Wu et al 2015). Moreover, NEAT1_2 was found to inhibit cellular proliferation (Wu et al 2015).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Neat1 is a p53-inducible lincRNA essential for transformation suppression

et al. 2017

View full text Add to dashboard Cite

The p53 gene is mutated in over half of all cancers, reflecting its critical role as a tumor suppressor. Although p53 is a transcriptional activator that induces myriad target genes, those p53-inducible genes most critical for tumor suppression remain elusive. Here, we leveraged p53 ChIP-seq (chromatin immunoprecipitation [ChIP] combined with high-throughput sequencing) and RNA-seq (RNA sequencing) data sets to identify new p53 target genes, focusing on the noncoding genome. We identify Neat1, a noncoding RNA (ncRNA) constituent of paraspeckles, as a p53 target gene broadly induced by mouse and human p53 in different cell types and by diverse stress signals. Using fibroblasts derived from Neat1 −/− mice, we examined the functional role of Neat1 in the p53 pathway. We found that Neat1 is dispensable for cell cycle arrest and apoptosis in response to genotoxic stress. In sharp contrast, Neat1 plays a crucial role in suppressing transformation in response to oncogenic signals. Neat1 deficiency enhances transformation in oncogene-expressing fibroblasts and promotes the development of premalignant pancreatic intraepithelial neoplasias (PanINs) and cystic lesions in Kras G12D -expressing mice. Neat1 loss provokes global changes in gene expression, suggesting a mechanism by which its deficiency promotes neoplasia. Collectively, these findings identify Neat1 as a p53-regulated large intergenic ncRNA (lincRNA) with a key role in suppressing transformation and cancer initiation, providing fundamental new insight into p53-mediated tumor suppression.

show abstract

Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Neat1 is a p53-inducible lincRNA essential for transformation suppression

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Xie et al showed lncRNA TUG1 contributed to tumorigenesis of human osteosarcoma by sponging miR-9-5p and regulating POU2F1 expression [21]. NEAT1 (nuclear enriched abundant transcript 1) is a newly identified nuclear-restricted lncRNA, which has earned the reputation as a transcriptional regulator for numerous genes [22]. Recent studies showed that NEAT1 dysregulation promoted tumorigenesis in a variety of human cancers.…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: LncRNA NEAT1 regulates epithelial-mesenchymal transition of osteosarcoma by miR-186-5p as competing endogenous RNA

H¹,

Zhao²

2017

Oncotarget

View full text Add to dashboard Cite

Increasing evidence showed that lncRNA NEAT1 play important roles in regulating tumor carcinogenesis and progression. However, the function and underlying mechanism of NEAT1 in osteosarcoma (OS) remain unclear. In the present study, we found that NEAT1 expression was significantly upregulated in OS tissues and cell lines. High NEAT1 expression was closely associated with advanced clinicopathologic features and poor overall survival of OS patients. In vitro function assay, we found that NEAT1 could promote OS cells proliferation, invasion, and epithelial-mesenchymal transition (EMT) process. NEAT1 could also promote OS cells growth in vivo. In addition, our studies showed that miR-186-5p was a downstream target of NEAT1 in OS. Functionally, miR-186-5p suppressed OS cells proliferation, invasion, and EMT process. Furthermore, our data revealed that HIF-1α was a downstream target of miR-186-5p and NEAT1 could exert its tumor oncogenic roles on OS cells via miR-186-5p/ HIF-1α axis. Taken together, we elucidated that the NEAT1/miR-186-5p/HIF-1α axis might be a therapeutic approach for the treatment of OS.

show abstract

“…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.…”

Section: Introductionmentioning

confidence: 99%

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

Chen

Cai

Wang³

et al. 2018

Clinical Cancer Research

284

240

View full text Add to dashboard Cite

Purpose: Long noncoding RNAs have been implicated in gliomagenesis, but their mechanisms of action are mainly undocumented. Through public glioma mRNA expression data sets, we found that NEAT1 was a potential oncogene. We systematically analyzed the clinical significance and mechanism of NEAT1 in glioblastoma.Experimental Design: Initially, we evaluated whether NEAT1 expression levels could be regulated by EGFR pathway activity. We subsequently evaluated the effect of NEAT1 on the WNT/ b-catenin pathway and its target binding gene. The animal model supported the experimental findings.Results: We found that NEAT1 levels were regulated by EGFR pathway activity, which was mediated by STAT3 and NFkB (p65) downstream of the EGFR pathway. Moreover, we found that NEAT1 was critical for glioma cell growth and invasion by increasing b-catenin nuclear transport and downregulating ICAT, GSK3B, and Axin2. Taken together, we found that NEAT1 could bind to EZH2 and mediate the trimethylation of H3K27 in their promoters. NEAT1 depletion also inhibited GBM cell growth and invasion in the intracranial animal model.Conclusions: The EGFR/NEAT1/EZH2/b-catenin axis serves as a critical effector of tumorigenesis and progression, suggesting new therapeutic directions in glioblastoma. Clin Cancer Res; 1-12.Ó2017 AACR.

show abstract

Nuclear-enriched abundant transcript 1 as a diagnostic and prognostic biomarker in colorectal cancer

Cited by 125 publications

References 52 publications

Neat1 is a p53-inducible lincRNA essential for transformation suppression

Neat1 is a p53-inducible lincRNA essential for transformation suppression

WITHDRAWN: LncRNA NEAT1 regulates epithelial-mesenchymal transition of osteosarcoma by miR-186-5p as competing endogenous RNA

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

Contact Info

Product

Resources

About