Dataset Information

LncRNA MAGI2-AS3 inhibits bladder cancer progression by targeting the miR-31-5p/TNS1 axis.

ABSTRACT: In this study, we performed bioinformatics analysis to identify the competing endogenous RNAs (ceRNAs) that regulate bladder cancer (BCa) progression. RNA-sequencing data analysis identified 2451 differentially expressed mRNAs, 174 differentially expressed lncRNAs, and 186 microRNAs (miRNAs) in BCa tissues (n=414) compared to the normal urothelial tissues (n=19) from the TGCA database. CeRNA network analysis of the differentially expressed lncRNAs and mRNAs showed strong positive correlation between lncRNA MAGI2-AS3 and Tensin 1 (TNS1) mRNA in BCa tissues. Bioinformatics analysis also showed that both MAGI2-AS3 and TNS1 mRNA sequences contain miR-31-5p binding sites. Furthermore, we observed significantly lower MAGI2-AS3 and TNS1 mRNA expression and higher miR-31-5p expression in the BCa tissues and cell lines (T24 and J82) compared with their corresponding controls. Functional and biochemical experiments in BCa cell lines including luciferase reporter assays showed that MAGI2-AS3 upregulated TNS1 by sponging miR-31-5p. Transwell assays showed that the MAGI2-AS3/miR-31-5p/TNS1 axis regulated migration and invasion ability of BCa cell lines. Moreover, immunohistochemical staining of paired BCa and normal urothelial tissues showed that low expression of TNS1 correlated with advanced tumor (T) stages and lymph node metastasis in BCa. In conclusion, our study demonstrates that the MAGI2-AS3/miR-31-5p/TNS1 axis regulates BCa progression.

SUBMITTER: Tang C

PROVIDER: S-EPMC7803496 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

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LncRNA MAGI2-AS3 inhibits bladder cancer progression by targeting the miR-31-5p/TNS1 axis.

Tang Congyi C Cai Yi Y Jiang Huichuan H Lv Zhengtong Z Yang Changzhao C Xu Haozhe H Li Zhi Z Li Yuan Y

Aging 20201120 24

In this study, we performed bioinformatics analysis to identify the competing endogenous RNAs (ceRNAs) that regulate bladder cancer (BCa) progression. RNA-sequencing data analysis identified 2451 differentially expressed mRNAs, 174 differentially expressed lncRNAs, and 186 microRNAs (miRNAs) in BCa tissues (n=414) compared to the normal urothelial tissues (n=19) from the TGCA database. CeRNA network analysis of the differentially expressed lncRNAs and mRNAs showed strong positive correlation bet ...[more]

PMID: 33231563

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Project description:BackgroundLung cancer is a malignant tumor that seriously threatens the health of human beings. Long non-coding RNAs (lncRNAs) are thought to play important roles in the pathophysiology of lung cancer. In this study, we identified a new lncRNA, MAGI2-AS3 in non-small cell lung cancer (NSCLC) tissues by conducting an integrated bioinformatics analysis. Mechanistic studies were also performed to explore the biological functions of MAGI2-AS3 in NSCLC progression.MethodsA bioinformatics analysis was conducted to determine the prognostic role of MAGI2-AS3. CCK-8, EdU assay, colony formation and Transwell were performed to determine the effects of MAGI2-AS3 on the progression of NSCLC cells. A nude mice model was used to evaluate the effects of MAGI2-AS2 on the in vivo tumor growth of NSCLC. Luciferase reporter and RNA pull-down assays were used to evaluate interactions between MAGI2-AS3 and its downstream targets.ResultsMAGI2-AS3 was found to be downregulated in NSCLC tissues. The gain-of-function in vitro studies showed that the overexpression of MAGI2-AS3 suppressed NSCLC cell proliferation and invasion. Conversely, the knockdown of MAGI2-AS3 had the opposite effects. The bioinformatics analysis and luciferase report assay revealed that MAGI2-AS3 functioned as competing endogenous RNA to suppress microRNA (miR)-629-5p expression, while miR-629-5p suppressed thioredoxin-interacting protein (TXNIP) expression by targeting its 3' untranslated region. The rescue experiment results showed that MAGI2-AS3 knockdown enhanced NSCLC cell progression (increasing cell proliferation and invasion, but reducing cell apoptosis), which was counteracted by miR-629-5p inhibition or TXNIP overexpression.ConclusionsThe study revealed that MAGI2-AS3 was downregulated in NSCLC tissues and cells, and MAGI2-AS3 suppressed NSCLC cell progression. Further, the mechanistic results showed that MAGI2-AS3 exerted a tumor-suppressive effect in NSCLC by targeting the miR-629-5p/TXNIP axis.

Project description:Retinoblastoma (RB) is the most common intraocular tumor in childhood. Long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NTAT1) has been reported to be related to RB progression. This study aims to study the molecular mechanism of NEAT1 in regulating cell cycle, proliferation, apoptosis, migration, and invasion in RB. The expression levels of NEAT1 and miR-3619-5p were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein expression of LIM and SH3 domain protein 1 (LASP1) was measured by western blot. The proliferation of RB cells was analyzed by cell counting kit-8 (CCK-8) and cell colony formation assays. Cell migration and invasion were evaluated by transwell assay. Cell cycle and apoptosis were assessed by flow cytometry analysis. The association between miR-3619-5p and NEAT1 or LASP1 was predicted by starBase 3.0 database and identified by dual-luciferase reporter assay. The effects of NEAT1 knockdown on the tumor growth in vivo were detected by in vivo tumor formation assay. NEAT1 expression was dramatically up-regulated, and miR-3619-5p expression was obviously downregulated in RB tissues and cells compared with control groups. The protein level of LASP1 was obviously increased in RB tissues or cells relative to paracancerous normal tissues or cells, respectively. Functionally, NEAT1 silencing inhibited RB cell migration, invasion, and proliferation, whereas induced cell apoptosis and cell cycle arrest in RB; this phenomenon was partially abolished by miR-3619-5p inhibitor. Mechanistically, NEAT1 acted as a sponge of miR-3619-5p, and miR-3619-5p was associated with LASP1. In addition, NEAT1 knockdown decreased the volume and weight of RB tumor in vivo. Together, NEAT1 silencing repressed cell migration, invasion, and proliferation, whereas induced cell apoptosis and cycle arrest by sponging miR-3619-5p to inhibit LASP1 expression in RB cells. This study may provide a theoretical basis for RB therapy.

Dataset Information

LncRNA MAGI2-AS3 inhibits bladder cancer progression by targeting the miR-31-5p/TNS1 axis.

Publications

LncRNA MAGI2-AS3 inhibits bladder cancer progression by targeting the miR-31-5p/TNS1 axis.

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