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LncRNA HCG11 promotes proliferation and migration in gastric cancer via targeting miR-1276/CTNNB1 and activating Wnt signaling pathway.

ABSTRACT: Background:Gastric cancer (GC) is one common cancer which occurs in the stomach leading to high mortality around the world. Long non-coding RNAs (lncRNAs) were found overexpressed or silenced in the occurrence and progression of multiple cancers including GC. Method:The gene expression level in GC tissues and cells were analyzed by RT-qPCR. CCK-8, colony formation, flow cytometry and transwell assays were performed for the function analysis of HLA complex group 11 (HCG11). The mechanism study for HCG11 was conducted using RIP, RNA pull down and luciferase reporter assays. Results:HCG11 was discovered highly expressed in GC tissues and cells. Depletion experiments were used to evaluate HCG11 silence on cell proliferation, migration and apoptosis. Moreover, Wnt signaling pathway was found as a tumor promoter in GC. RIP assay, RNA pull down assay and luciferase reporter assay were performed to illustrate the relationship of HCG11, miR-1276 and CTNNB1. Rescue assays revealed that HCG11/miR-1276/CTNNB1 axis regulated the incidence and development of GC. Tumor formation in mice proved that HCG11 was negatively correlated with miR-1276 and had positively correlation with CTNNB1. Conclusion:Overall, HCG11 accelerated proliferation and migration in GC through miR-1276/CTNNB1 and Wnt signaling pathway, revealing that HCG11 could be a brand new target for GC.

SUBMITTER: Zhang H

PROVIDER: S-EPMC6933929 | biostudies-literature |

REPOSITORIES: biostudies-literature

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[LncRNA LINC00342 regulates gastric cancer cell proliferation, migration and invasion by targeting miR-596].

Project description:ObjectiveTo investigate the expression levels of LINC00342 in gastric cancer (GC) tissues and cells and the pathways mediating its effects on biological behaviors of GC cells.MethodsBioinformatic analysis was performed to identify the lncRNAs and their downstream miRNAs involved in regulation of biological behaviors of GC cells. qRT-PCR was used to analyze the differential expression of LINC00342 and miR-596 in GC cell lines, human gastric mucosal cells, and GC and adjacent tissues. In human GC MGC-803 and MGC-823 cells, the effects of LINC00342 overexpression, miR-596 overexpression, LINC00342 knockdown, or miR-596 knockdown on cell proliferation, migration, invasion and cell cycle changes were examined using Edu assay, CCK-8 assay, wound healing assay, Transwell assay, and flow cytometry. The regulatory interaction between LINC00342 and miR-596 was investigated using a dual-luciferase reporter assay.ResultsInformatic analysis identified LINC00342 as the candidate lncRNA regulating biological behaviors of GC cells, with miR-596 as its downstream miRNA. LINC00342 expression levels were significantly higher while miR-596 expression levels were lower in GC tissues and cell lines than in the paired adjacent tissues and human gastric mucosal cell lines (all P<0.05). In MGC-803 and MGC-823 cells, overexpression of LINC00342 significantly enhanced cell proliferation (P<0.05), migration (P<0.01), and invasion (P<0.001) and reduced the percentage of G0/G1 phase cells (P<0.01), while knocking down LINC00342 significantly suppressed cell proliferation (P<0.05), migration (P<0.01), and invasion (P<0.001) and increased G0/G1 phase cell percentage (P<0.01). Modulation of miR-596 expression levels produced the opposite effects. Dual-luciferase reporter assay confirmed the specific binding between LINC00342 and miR-596 (P=0.0067).ConclusionIn GC cells, LINC00342 regulates cell proliferation, migration, and invasion by targeting miR-596.

| S-EPMC10630212 | biostudies-literature

LncRNA DLGAP1-AS1 accelerates glioblastoma cell proliferation through targeting miR-515-5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway.

Project description:IntroductionGlioblastoma (GBM), the primary malignant tumor in the central nervous system, features high aggressiveness and mortality. Long noncoding RNAs (lncRNAs) can exert the crucial function in regulating various human diseases, including GBM. However, the function and mechanism of lncRNA DLGAP1 antisense RNA 1 (DLGAP1-AS1) in GBM remain still unknown.MethodsDLGAP1-AS1 expression in GBM cells was detected by RT-qPCR. Functional assays were conducted to determine GBM cell proliferation and apoptosis. RIP, RNA pull down, and luciferase reporter assay were applied for measuring the interplay of DLGAP1-AS1 with other RNAs.ResultsDLGAP1-AS1 was distinctly upregulated in GBM cells. DLGAP1-AS1 depletion inhibited cell proliferation, but induced apoptosis. MiR-515-5p could be sponged by DLGAP1-AS1 in GBM cells and to repress cell proliferation in GBM. Further, Rho-associated coiled-coil containing protein kinase 1 (ROCK1) and Nuclear factor erythroid-2 like 1 (NFE2L1) were confirmed as the target gene of miR-515-5p. Wnt signaling pathway could be activated by DLGAP1-AS1 via regulating ROCK1 and NFE2L1 expression. Rescue assays proved that overexpression of both ROCK1 and NFE2L1 could totally reverse the inhibitory effect of silencing DLGAP1-AS1 on GBM cell proliferation.ConclusionLncRNA DLGAP1-AS1 accelerated cell proliferation in GBM via targeting miR-515-5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway.

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LncRNA HCG11/miR-26b-5p/QKI5 feedback loop reversed high glucose-induced proliferation and angiogenesis inhibition of HUVECs.

Project description:Acute coronary syndrome caused by the rupture of atherosclerotic plaques is one of the primary causes of cerebrovascular and cardiovascular events. Neovascularization within the plaque is closely associated with its stability. Long non-coding RNA (lncRNA) serves a crucial role in regulating vascular endothelial cells (VECs) proliferation and angiogenesis. In this study, we identified lncRNA HCG11, which is highly expressed in patients with vulnerable plaque compared with stable plaque. Then, functional experiments showed that HCG11 reversed high glucose-induced vascular endothelial injury through increased cell proliferation and tube formation. Meanwhile, vascular-related RNA-binding protein QKI5 was greatly activated. Luciferase reporter assays and RNA-binding protein immunoprecipitation (RIP) assays verified interaction between them. Interestingly, HCG11 can also positively regulated by QKI5. Bioinformatics analysis and luciferase reporter assays showed HCG11 can worked as a competing endogenous RNA by sponging miR-26b-5p, and QKI5 was speculated as the target of miR-26b-5p. Taken together, our findings revered that the feedback loop of lncRNA HCG11/miR-26b-5p/QKI-5 played a vital role in the physiological function of HUVECs, and this also provide a potential target for therapeutic strategies of As.

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HCG11 up-regulation induced by ELK4 suppressed proliferation in vestibular schwannoma by targeting miR-620/ELK4.

Project description:BackgroundVestibular schwannoma (VS) is a kind of benign tumor deriving from the acoustic nerve sheath. Substantial long non-coding RNAs (lncRNAs) were illustrated to have crucial roles in multiple cancers. However, few lncRNAs were elucidated in VS.MethodsHCG11, miR-620 and ELK4 expression were tested by RT-qPCR. Gain-of-function experiments were conducted to confirm the effect of HCG11 on VS.ResultsHCG11 possessed a low expression in VS cell lines. Overexpression of HCG11 repressed cell proliferation but accelerated apoptosis of VS cells. Moreover, we identified ELK4 stimulated the transcription of HCG11 and their affinity was verified by ChIP assays. MiR-620 was chosen to be a target of HCG11 and it was tested to have a high expression in VS cell lines. Moreover, depletion of miR-620 could inhibit cell proliferative ability while fostering apoptosis rate of VS cells. ELK4 was low expressed in VS cell lines and knockdown of ELK4 could rescue the effects made by HCG11 overexpression on progression of VS.ConclusionsHCG11 could inhibit the growth of VS by targeting miR-620/ELK4 in VS cells. HCG11 was a novel therapeutic target for VS treatment.

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Onco-miR-130 promotes cell proliferation and migration by targeting TGFβR2 in gastric cancer.

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LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β-catenin signaling pathway.

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| S-EPMC7434752 | biostudies-literature

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