Decreased expression of the long non-coding RNA MLLT4 antisense RNA 1 is a potential biomarker and an indicator of a poor prognosis for gastric cancer

Lai, Yuexing; Xu, Ping; Liu, Jie; Li, Qinghua; Ren, Dianxu; Zhang, Jun; Wang, Jing

doi:10.3892/ol.2017.6478

Cited by 20 publications

(19 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Gastric cancer (GC) is one of the most common malignancies all over the world [1]. In East Asia countries, especially China, the incidence is up to 42% [2]. In recent years, the five-year total survival rate of GC patients is still not satisfactory, though gastric tumor diagnosis, surgical techniques and novel molecular targeting drugs have significantly improved [3].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway

et al. 2018

View full text Add to dashboard Cite

In this study, we aimed to investigate the effects of lncRNA CASC11 on gastric cancer (GC) cell progression through regulating miR-340-5p and cell cycle pathway. Expressions of lncRNA CASC11 in gastric cancer tissues and cell lines were determined by qRT-PCR. Differentially expressed lncRNAs, mRNAs and miRNAs were screened through microarray analysis. The relationship among CASC11, CDK1 and miR-340-5p was predicted by TargetScan and validated through dual luciferase reporter assay. Western blot assay examined the protein level of CDK1 and several cell cycle regulatory proteins. GO functional analysis and KEGG pathway analysis were used to predict the association between functions and related pathways. Cell proliferation was determined by CCK-8 assays. Cell apoptosis and cell cycle were detected by flow cytometry assay. CASC11 was highly expressed in GC tissues and cell lines. Knockdown of CASC11 inhibited GC cell proliferation, promoted cell apoptosis and blocked cell cycle. KEGG further indicated an enriched cell cycle pathway involving CDK1. QRT-PCR showed that miR-340-5p was down-regulated in GC cells tissues, while CDK1 was up-regulated. Furthermore, CASC11 acted as a sponge of miR-340-5p which directly targeted CDK1. Meanwhile, miR-340-5p overexpression promoted GC cell apoptosis and induced cell cycle arrest, while CDK1 overexpression inhibited cell apoptosis and accelerated cell cycle. Our study revealed the mechanism of CASC11/miR-340-5p/CDK1 network in GC cell line, and suggested that CASC11 was a novel facilitator that exerted a biological effect by activating the cell cycle signaling pathway. This finding provides a potential therapeutic target for GC.

show abstract

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway

et al. 2018

View full text Add to dashboard Cite

show abstract

“…22 For instance, lncRNA MALAT1 can promote osteosarcoma metastasis and proliferation by sponging miR-144-3p. 29 LncRNA TRERNA1 can promote GC progression by regulating EMT and enhancing SNAI1 expression. 26 LncRNA SNHG17 is able to promote cell proliferation by acting as an unfavorable prognostic indicator and epigenetically inhibiting P57 in colorectal cancer.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Tan

Wang

Liu

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

Accumulating evidence has indicated that lncRNA NEAT1 exerts critical roles in cancers. So far, the detailed biological role and mechanisms of NEAT1 which are responsible for human gastric cancer (GC) is still largely unknown. Here, we observed that NEAT1 and STAT3 expression were significantly upregulated in human gastric cancer cells including BGC823, SGC-7901, AGS, MGC803 and MKN28 cells compared to normal gastric epithelial cells GES-1 while miR-506 was downregulated. We inhibited NEAT1 and observed that NEAT1 inhibition was able to repress the growth, migration and invasion of gastric cancer cells. Reversely, overexpression of NEAT1 exhibited an increase ability of gastric cancer progression in BGC823 and SGC-7901 cells. Bioinformatics analysis, dual luciferase reporter assays, RIP assays and RNA pull-down tests validated the negative binding correlation between NEAT1 and miR-506. In addition, it was found that miR-506 can modulate expression of NEAT1 in vitro. STAT3 was predicted as an mRNA target of miR-506 and miR-506 mimics can suppress STAT3 mRNA expression. Subsequently, it was observed that downregulation of NEAT1 can restrain gastric cancer development by decreasing STAT3 which can be reversed by miR-506 inhibitors. Therefore, it was hypothesized in our study that NEAT1 can be recognized as a ceRNA to modulate STAT3 by sponging miR-506 in gastric cancer. In conclusion, we implied that NEAT1 can serve as an important biomarker in gastric cancer diagnosis and treatment. This article is protected by copyright. All rights reserved.

show abstract

“…With the development of high-throughput sequencing technology and bioinformatics, lncRNAs have been revealed to be involved in the development of numerous diseases, particularly tumors ( 36 – 39 ). However, the study of lncRNA expression profiles in LUAD has gradually increased.…”

Section: Discussionmentioning

confidence: 99%

Identification of ceRNA network based on a RNA‑seq shows prognostic lncRNA biomarkers in human lung adenocarcinoma

Ran

et al. 2018

Oncol Lett

View full text Add to dashboard Cite

Previous studies have emphasized the significant functions of long non-coding RNAs (lncRNAs) as competing endogenous RNAs (ceRNAs) in tumor biology. However, the functions of certain cancer lncRNAs in the lncRNA-related ceRNA network in lung adenocarcinoma (LUAD) are unknown. A systematic and integrative survey of RNA-seq data from The Cancer Genome Atlas (TCGA) was performed to identify candidate lncRNAs for the prognosis of LUAD. In total, 20,502 genes that contain 181 lncRNAs were evaluated in a cohort of 570 LUAD cases. Initially, 6,280 differentially expressed genes (fold-change >2, P<0.05) were obtained using R package, which includes 75 lncRNAs. Next, by univariate regression and multivariate Cox proportional hazards analysis, 32 genes were associated with survival in LUAD. Using these 29 mRNAs and 3 lncRNAs, a prognosis index (PI) was calculated to accurately estimate the survival in LUAD: PI=∑exprisk gene × HRrisk gene. Furthermore, the 32-gene signature was an independent prognostic indicator for LUAD (HR >1; P<0.05, by multivariate analysis). Weighted gene co-expression network analysis (WGCNA) of three risk lncRNAs-FAM138B, NHEG1 and TLX1NB-was performed, based on the P-values of the associated genes, and the top 27 miRNAs that bound to these lncRNAs were predicted by Miranda as target miRNAs. Next, these target miRNAs were transferred to the TarBase, miRTarBase, miRecards and starBase v2.0 databases to obtain their target genes. According to the previous miRNA-mRNA and miRNA-lncRNA data, three lncRNA-miRNA-mRNA ceRNA networks were established, based on the 29 prognostic mRNAs, forming a regulatory network in LUAD. The present study provided insight into the lncRNA-related ceRNA network in LUAD and has identified potential diagnostic and prognostic biomarkers.

show abstract

Decreased expression of the long non-coding RNA MLLT4 antisense RNA 1 is a potential biomarker and an indicator of a poor prognosis for gastric cancer

Cited by 20 publications

References 33 publications

RETRACTED ARTICLE: LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway

RETRACTED ARTICLE: LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Identification of ceRNA network based on a RNA‑seq shows prognostic lncRNA biomarkers in human lung adenocarcinoma

Contact Info

Product

Resources

About