LINC01018 and SMIM25 sponged miR-182-5p in endometriosis revealed by the ceRNA network construction

Jiang, Li; Zhang, Mengmeng; Wang, Sixue; Xiao, Yuzhen; Wu, Jingni; Zhou, Yuxin

doi:10.1177/2058738420976309

Cited by 12 publications

(6 citation statements)

References 56 publications

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“…PELATON is a long noncoding RNA also known as long intergenic nonprotein coding RNA 1272 ( LINC01272 ), small integral membrane protein 25 ( SMIM25 ), or GC-related lncRNA 1 ( GCRL1 ). A handful of reports indicated that PELATON has dual functions as an oncogene or a suppressor gene by acting as a miRNA sponge ( 53 , 55 , 56 ). PELATON promotes metastasis of colorectal cancer or gastric cancer by targeting the miR-876 /ITGB2 axis ( 53 ) or miR-885- 3p/CDK4 ( 52 ).…”

Section: Discussionmentioning

confidence: 99%

LncRNA PELATON, a Ferroptosis Suppressor and Prognositic Signature for GBM

Zhang

et al. 2022

Front. Oncol.

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PELATON is a long noncoding RNA also known as long intergenic nonprotein coding RNA 1272 (LINC01272). The known reports showed that PELATON functions as an onco-lncRNA or a suppressor lncRNA by suppressing miRNA in colorectal cancer, gastric cancer and lung cancer. In this study, we first found that PELATON, as an onco-lncRNA, alleviates the ferroptosis driven by mutant p53 and promotes mutant p53-mediated GBM proliferation. We also first confirmed that PELATON is a new ferroptosis suppressor lncRNA that functions as a ferroptosis inhibitor mainly by mutant P53 mediating the ROS ferroptosis pathway, which inhibits the production of ROS, reduces the levels of divalent iron ions, promotes the expression of SLC7A11, and inhibits the expression of ACSL4 and COX2.PELATON can inhibit the expression of p53 in p53 wild-type GBM cells and regulate the expression of BACH1 and CD44, but it has no effect on p53, BACH1 and CD44 in p53 mutant GBM cells. PELATON and p53 can form a complex through the RNA binding protein EIF4A3. Knockdown of PELATON resulted in smaller mitochondria, increased mitochondrial membrane density, and enhanced sensitivity to ferroptosis inducers to inhibit GBM cell proliferation and invasion. In addition, we established a favourite prognostic model with NCOA4 and PELATON. PELATON is a promising target for the prognosis and treatment of GBM.

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Section: Discussionmentioning

confidence: 99%

LncRNA PELATON, a Ferroptosis Suppressor and Prognositic Signature for GBM

Zhang

et al. 2022

Front. Oncol.

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“…Among these differentially expressed genes, the top four down-regulated lncRNAs were SMIM25, FENDRR, SFTA1P, and LINC01936 ( Table 2 ) and the top four up-regulated ones were LINC01133, CASC9, SOX21-AS1, and ESRG ( Table 3 ). After searching the literatures, we found that seven genes, except for LINC01936, were all contributed to the development of lung cancer by several pathways ( Chang et al, 2020 ; Gao et al, 2019 ; Jafari et al, 2022 ; Jiang et al, 2020 ; Ning et al, 2021 ; Wang et al, 2021a ; Xiong et al, 2019 ). Due to this, LINC01936 was used for further analysis.…”

Section: Resultsmentioning

confidence: 99%

LINC01936 inhibits the proliferation and metastasis of lung squamous cell carcinoma probably by EMT signaling and immune infiltration

Tian,

Liu,

et al. 2023

PeerJ

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Purpose To discover the biological function and potential mechanism of LINC01936 in the development of lung squamous cell carcinoma (LUSC). Methods Transcriptome data of LUSC from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to analyze the differentially expressed lncRNAs in LUSC and normal tissues by R “DEseq2”, “edgeR” and “limma” packages. The subcellular localization of LINC01936 was predicted by lncLocator. Cell proliferation and apoptosis were measured by CCK-8, MTT assay and Hoechst fluorescence staining. The migration and invasion were detected by Transwell assay. The function and pathway enrichment analysis were performed by Gene Ontology (GO) terms, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and gene set variation analysis (GSVA). The downstream targets of LINC01936 were predicted using RNA-Protein Interaction Prediction (RPISeq) program. The effect of LINC01936 on tumor immune infiltration was analyzed using Pearson Correlation Analysis using R “ggpubr” package. Results Based on the gene expression data of LUSC from TCGA database, 1,603, 1,702 and 529 upregulated and 536, 436 and 630 downregulated lncRNAs were obtained by DEseq2, edgeR and limma programs, respectively. For GSE88862 dataset, we acquired 341 differentially expressed lncRNAs (206 upregulated and 135 downregulated). Venn plot for the intersection of above differential expressed lncRNAs showed that there were 29 upregulated and 23 downregulated genes. LINC01936 was one of downregulated lncRNAs in LUSC tissues. The biological analysis showed that the overexpression of LINC01936 significantly reduced proliferation, migration and invasion of LUSC cells, and promoted cell apoptosis. The knockdown of LINC01936 promoted cell proliferation and metastasis. Pathway and GSVA analysis indicated that LINC01936 might participated in DNA repair, complement, cell adhesion and EMT, etc. LINC01936 was predicted to interact with TCF21, AOC3, RASL12, MEOX2 or HSPB7, which are involved in EMT and PI3K-AKT-MTOR pathway, etc. The expression of LINC01936 was also positively correlated with the infiltrating immune cells in LUSC. Conclusions LINC01936 is downregulated in LUSC. LINC01936 affected proliferation, migration and invasion of LUSC cells probably by EMT and immune infiltration, which might serve as a new target for the treatment of LUSC.

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“…Emerging evidence supports the notion that miRNA can complement and bind to target genes and directly cut mRNA, so as to regulate the level of target mRNA[ 48 , 49 ]. The underlying mechanism for the role of miRNA-182-5p was further examined herein.…”

Section: Discussionmentioning

confidence: 96%

MiRNA-182-5p aggravates experimental ulcerative colitis via sponging Claudin-2

et al. 2021

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Tight junction proteins play crucial roles in maintaining the integrity of intestinal mucosal barrier. MiRNA-182-5p is capable of targeting claudin-2 which is one of the vital tight junction proteins and the effect and mechanism of miRNA-182-5p was explored here in the DSS-induced colitis model. The pathological conditions were evaluated via hematoxylin and eosin staining. The gene expression level was assessed via PCR. Quantitative immunohistochemistry analysis was performed for the measurement of claudin-2. microRNA.org online tool was used for target gene prediction. Luciferase reporter assay and RNA pull-down assay were performed to detect the target of miRNA-182-5p. The inflammatory and oxidative stress level were measured using corresponding kits. MiRNA-182-5p was highly expressed in colitis model and miRNA-182-5p inhibitor exerted protective effects on colitis induced by DSS in mice. The protective effects includded improvement of pathological changes, increases in anti-inflammation and anti-oxidative genes, and up-regulation of TGF-β1. Claudin-2 mRNA was predicted as the target of miRNA-182-5p, which was validated via luciferase reporter assay and RNA pull-down assay. Claudin-2 overexpression was found in miRNA-182-5p inhibitor group. Consistent with the role of miRNA-182-5p, claudin-2 overexpression also exerted protective effects on DSS-induced colitis in mice. Inhibition of miRNA-182-5p exerted protective effects on colitis via targeting and upregulating claudin-2. The findings in study provide a new therapeutic strategy for colitis treatment and lay the foundation for future study.

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LINC01018 and SMIM25 sponged miR-182-5p in endometriosis revealed by the ceRNA network construction

Cited by 12 publications

References 56 publications

LncRNA PELATON, a Ferroptosis Suppressor and Prognositic Signature for GBM

LncRNA PELATON, a Ferroptosis Suppressor and Prognositic Signature for GBM

LINC01936 inhibits the proliferation and metastasis of lung squamous cell carcinoma probably by EMT signaling and immune infiltration

MiRNA-182-5p aggravates experimental ulcerative colitis via sponging Claudin-2

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