LncRNA miR143HG suppresses miR‐21 through methylation to inhibit cell invasion and migration

Wu, Xun; Cen, Wei; Yu, Dahai; Huaqing, Wei; Su, Jiping; Guo, Mengzhu; Meng, Na

doi:10.1002/lary.28474

Cited by 14 publications

(11 citation statements)

References 18 publications

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“…35 Xun et al found that lncRNA miR143HG epigenetically suppresses miR-21 expression in EC cells via DNA methylation. 36 Cheng et al found that lncRNA HOTAIR mediated miR-122 expression via DNMTs-mediated DNA methylation. 37 In this study, overexpression of LOC441178 decreased the level of miR-182 in ESCC cells.…”

Section: Dovepressmentioning

confidence: 99%

<p>LOC441178 Overexpression Inhibits the Proliferation and Migration of Esophageal Carcinoma Cells via Methylation of miR-182</p>

Chen

et al. 2020

OTT

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Background Long noncoding RNAs (lncRNAs) have been shown to play an important role in the development and progression of esophageal carcinoma (EC). Recently, lncRNA LOC441178 was shown to be dysregulated in many cancer types; however, the role of LOC441178 in EC remains unclear. Materials and Methods Flow cytometry, transwell and wound healing assays were used to measure the apoptosis and migration in esophageal squamous cell carcinoma (ESCC) cells. RT-qPCR was used to detect the level of miR-182 in LOC441178-overexpressed EC cells. In addition, DNA methylation status of miR-182 promoter in LOC441178-overexpressed ESCC cells was detected by methylation-specific PCR (MSP) and bisulfite sequencing PCR. Results In this study, we found that LOC441178 negatively regulated miR-182 expression in ESCC cells. In addition, overexpression of LOC441178 inhibited the proliferation and migration and induced apoptosis in ESCC cells via downregulation of miR-182. Moreover, overexpression of LOC441178 markedly inhibited the phosphorylation of Akt and phosphorylation FOXO3a and increased the expression of FOXO3a in ESCC cells via downregulation of miR-182. Mechanistically, LOC441178 overexpression epigenetically suppressed miR-182 expression via DNA methylation. In vivo experiments revealed that overexpression of LOC441178 inhibited ESCC tumor growth in mouse xenograft model. Conclusion Collectively, our data suggested that LOC441178 overexpression epigenetically inhibited tumorigenesis of ESCC via DNA methylation of miR-182. These data indicated that the LOC441178/miR-182 axis might represent a novel therapeutic option for the treatment of ESCC.

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Section: Dovepressmentioning

confidence: 99%

<p>LOC441178 Overexpression Inhibits the Proliferation and Migration of Esophageal Carcinoma Cells via Methylation of miR-182</p>

Chen

et al. 2020

OTT

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“…Xie et al (Xie et al, 2019) suggested that lncRNA MIR143HG inactivates Wnt/beta‐catenin pathway through regulation of miR‐1275/AXIN2 axis, thereby arresting the malignant development of bladder cancer. As reported, lncRNA MIR143HG in laryngeal squamous cell carcinoma restrains miR‐21 expression to retard invasion and migration of tumor cells through methylation (Xun et al, 2020). LncRNA LINC00702 hinders NSCLC proliferation and invasion by modulating miR‐510/PTEN axis (Yu et al, 2019).…”

Section: Discussionmentioning

confidence: 78%

Identification of a dysregulated ceRNA network modulated by copy number variation‐driven lncRNAs in lung squamous cell carcinoma

Ding

Huang

et al. 2022

Environ and Mol Mutagen

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Lung cancer is primarily responsive for cancer death, and its progression is aggressively affected by copy number variation (CNV). Through bioinformatics approach, a ceRNA network of CNV-driven lncRNAs in lung squamous cell carcinoma (LUSC) patients was constructed. Data on normal and LUSC tumor tissue from The Cancer Genome Atlas (TCGA)-LUSC dataset were subjected to differential analysis, and differentially expressed lncRNAs (DElncRNAs), DEmiRNAs, and DEmRNAs were obtained. Based on TCGA-LUSC, CNVs of normal and tumor tissue samples were then compared using a Chi-square test, and lncRNAs were intersected based on their CNVs and expression alternation. In combination with the Kruskal-Wallis test, CNVdriven lncRNAs were acquired. Afterwards, miRNAs and mRNAs that interacted with CNV-driven lncRNAs were obtained based on databases (LncBase, starBase, miRDB, mirDIP and TargetScan), DElncRNAs, DEmiRNAs and DEmRNAs, and correlation analysis. The acquired lncRNAs, miRNAs and mRNAs were subjected to Cytoscape software to construct a CNV-driven ceRNA network, which involved 5 lncRNAs (MIR143HG, LINC00702, MIR22HG, RP11-180 N14.1, RP11-473 M20.9), 6 miRNAs (miR-3200-3p, miR-1301-3p, miR-93-3p, miR-96-5p, miR-96-5p, miR-130b-5p, miR-205-5p) and 80 mRNAs. Kyoto Encyclopedia of Genes and Genomes and Gene Ontology enrichment analyses indicated that downstream mRNAs were mainly correlated with blood vessel development and T cell-mediated immunity. In summary, we devoted to analyzing CNV-related lncRNAs, mRNAs, and miRNAs in LUSC, thus clarifying 5 lncRNAs that may influence the malignant progression of LUSC. The ceRNA network regulated by these lncRNAs may be the novel pathogenesis of LUSC.

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“…In Human LSCC cell line UM-SCC-17A, the overexpression of miR143HG led to the downregulation of miR-21 expression, while the overexpression of miR-21 did not affect miR143HG. Furthermore, recent studies also have confirmed that overexpression of miR143HG leads to an increase in miR-21 methylation and a decrease in the rate of migration and invasion of LSCC cells (Xun et al, 2019).…”

Section: Other Types Of Lncrnamentioning

confidence: 81%

Regulatory Mechanisms of lncRNAs and Their Target Gene Signaling Pathways in Laryngeal Squamous Cell Carcinoma

Chen

Nie

2020

Front. Pharmacol.

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Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumor that occurs in the head and neck. People living in areas with serious air pollution and those who smoke and drink for a long time belong to high-risk groups. Although great progress has been made in chemotherapy, radiotherapy, and molecular targeted therapy in recent years, the prognosis of patients is still not good. The proliferation, invasion, and apoptosis of LSCC are controlled by many factors, which are the key factors influencing the prognosis of patients. Previous researches have demonstrated that long noncoding RNAs (lncRNAs) can be used as oncogenes or tumor suppressor genes in the occurrence and development of cancer and regulate cancer through various ways including epigenetic regulation and post-transcriptional regulation. The characteristics and roles of lncRNAs in LSCC, however, are not clear. In this review, we will discuss the role and function of lncRNAs in the proliferation, invasion, and apoptosis of LSCC and analyze the relationship between lncRNAs and lncRNA-regulated signaling pathways in LSCC pathological process. The difficulties faced by the related research of LSCC are discussed. It provides reference ideas for the molecular mechanism research of LSCC targeting lncRNA and its signaling pathways, the development of clinical prevention and therapeutic drug and individualized treatment, thereby improving the quality of life of patients.

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LncRNA miR143HG suppresses miR‐21 through methylation to inhibit cell invasion and migration

Cited by 14 publications

References 18 publications

<p>LOC441178 Overexpression Inhibits the Proliferation and Migration of Esophageal Carcinoma Cells via Methylation of miR-182</p>

<p>LOC441178 Overexpression Inhibits the Proliferation and Migration of Esophageal Carcinoma Cells via Methylation of miR-182</p>

Identification of a dysregulated ceRNA network modulated by copy number variation‐driven lncRNAs in lung squamous cell carcinoma

Regulatory Mechanisms of lncRNAs and Their Target Gene Signaling Pathways in Laryngeal Squamous Cell Carcinoma

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