ArticleOncoTargets and therapy2019
LncRNA RP11-422N16.3 Inhibits Cell Proliferation and EMT, and Induces Apoptosis in Hepatocellular Carcinoma Cells by Sponging miR-23b-3p.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- MicroRNA-23b: Roles, functions and mechanisms in tumor.Genes & diseases · 2026Review
- Epithelial to Mesenchymal Transition Transcriptional Regulator ZEB1 in Liver Cancer: Oncogenic Roles and Therapeutic Potential.International journal of molecular sciences · 2025Review
- RP11-Derived Long Non-Coding RNAs in Hepatocellular Carcinoma: Hidden Treasures in Plain Sight.Oncology research · 2025Review
- Transcriptomic and genomic characteristics of intrahepatic metastases of primary liver cancer.BMC cancer · 2024Article
- Evaluating the Role of lncRNAs in the Incidence of Cardiovascular Diseases in Androgenetic Alopecia Patients.Cardiovascular toxicology · 2022Review
- LncRNA prostate androgen-regulated transcript 1 (PART 1) functions as an oncogene in osteosarcoma via sponging miR-20b-5p to upregulate BAMBI.Annals of translational medicine · 2021Article
- Promotor Hypomethylation Mediated Upregulation of miR-23b-3p Targets PTEN to Promote Bronchial Epithelial-Mesenchymal Transition in Chronic Asthma.Frontiers in immunology · 2021Article
- The Role of miR-23b in Cancer and Autoimmune Disease.Journal of oncology · 2021Review
- Modulation of the TGF-β signaling pathway by long noncoding RNA in hepatocellular carcinoma.Biomarker research · 2020Review
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
objectiveThis study investigated the mechanism of RP11-422N16.3 sponging miR-23b-3p in cell proliferation, apoptosis and epithelial-mesenchymal transition (EMT) in liver cancer.
methodsExpressions of RP11-422N16.3, miR-23b-3p and dimethylglycine dehydrogenase (DMGDH) were determined in liver cancer tissues, adjacent normal tissues, hepatocellular carcinoma cell lines and normal liver epithelial cell line. Up-regulation of RP11-422N16.3 and down-regulation of miR-23b-3p were conducted in hepatocellular carcinoma cells. Bioinformatics analysis, luciferase reporter assay and RNA-pull down assay were performed to verify the relationship among miR-23b-3p, DMGDH, as well as RP11-422N16.3. Cell proliferation and cell apoptosis were determined by CCK-8 and Flow Cytometry analysis, respectively.
resultsExpressions of RP11-422N16.3 and DMGDH were down-regulated while that of miR-23b-3p were up-regulated in hepatocellular carcinoma cancer tissues and cells. RP11-422N16.3 localized in cytoplasm and competitively bound to miR-23b-3p. Up-regulation of RP11-422N16.3 and down-regulation of miR-23b-3p contributed to increased expressions of DMGDH and E-cadherin, and decreased expressions of miR-23b-3p, ZEB1, Snail and Vimentin, resulting in inhibiting cell proliferation and promoting cell apoptosis. Inhibition of RP11-422N16.3 or overexpression of miR-23b-3p accelerated cell proliferation and slowed down cell apoptosis. miR-23b-3p inhibited the expression of DMGDH.
conclusionOur data suggested that LncRNA RP11-422N16.3, by competitively binding to miR-23b-3p, promoted DMGDH expression, contributing to inhibit cell proliferation and EMT, and induce cell apoptosis in hepatocellular carcinoma cells.
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