ArticleEBioMedicine2018
LncRNA HOTAIR epigenetically suppresses miR-122 expression in hepatocellular carcinoma via DNA methylation.
Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 165 citations in OpenAlex.
- A Three-Gene Prognostic Signature Driven by an ER Stress-Associated ceRNA Network: Integrating Single-Cell Transcriptomics and Cross-Platform Validation in Hepatocellular Carcinoma.Current issues in molecular biology · 2026Article
- Epigenetic Alterations in Hepatocellular Carcinoma: Mechanisms and Biomarkers for Precision Therapy.Cancers · 2026Review
- Decoding the functional landscape of long non-coding RNAs in hepatocellular carcinoma: molecular mechanisms, clinical implications, and therapeutic prospects.Journal of the Egyptian National Cancer Institute · 2026Review
- RNA Therapeutics in Viral Infections and Cancer: Mechanisms, Challenges, and Prospects: A Review.Pharmaceutics · 2026Review
- The lncRNA-DNA Methylation Axis in Hepatocellular Carcinoma: Mechanisms, Epigenetic Plasticity, and Biological Implications.Biology · 2026Review
- Small activating RNA AW1-51 (CEBPA-51) elicits targeted DNA demethylation to promote gene activation.bioRxiv : the preprint server for biology · 2025Article
- Perspectives on NcRNAs in HBV/cccDNA-driven HCC progression.Cancer cell international · 2025Review
- Macrophage polarization in hepatocellular carcinoma: a lncRNA-centric perspective on tumor progression and metastasis.Clinical and experimental medicine · 2025Review
- The Importance of Cancer Stem Cells and Their Pathways in Endometrial Cancer: A Narrative Review.Cells · 2025Review
- Epigenetic and epitranscriptomic role of lncRNA in carcinogenesis (Review).International journal of oncology · 2025Review
- Exploring the potential mechanisms of sorafenib resistance in hepatocellular carcinoma cell lines based on RNA sequencing.Cancer cell international · 2025Article
- Long Non-Coding RNAs in Non-Alcoholic Fatty Liver Disease; Friends or Foes?Cell biochemistry and biophysics · 2025Review
- The role of lncRNAs in the interplay of signaling pathways and epigenetic mechanisms in glioma.Epigenomics · 2025Review
- The interactive role of microRNA and other non-coding RNA in hepatitis B (HBV) associated fibrogenesis.Functional & integrative genomics · 2025Review
- Dual Roles of miR-10a-5p and miR-10b-5p as Tumor Suppressors and Oncogenes in Diverse Cancers.International journal of molecular sciences · 2025Review
- EZH2: From Oncogenic Driver to Therapeutic Target for Overcoming Drug Resistance in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2025Review
- Lipid Nanoparticles as a Platform for miRNA and siRNA Delivery in Hepatocellular Carcinoma.Current drug delivery · 2025Review
- miRNAs in HCC, pathogenesis, and targets.Hepatology (Baltimore, Md.) · 2024Article
- Deciphering the nexus between long non-coding RNAs and endoplasmic reticulum stress in hepatocellular carcinoma: biomarker discovery and therapeutic horizons.Cell death discovery · 2024Review
- Review
40 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNA-122 (miR-122), a pivotal liver-specific miRNA, is frequently repressed in hepatocellular carcinoma (HCC) and associated with poor prognosis. Long non-coding RNA (lncRNA) HOTAIR has been proved to function as an oncogene in multiple cancers including HCC. However, the relationship between HOTAIR and miR-122 in HCC remains largely unknown.
methodsWe investigated the function of HOTAIR and miR-122 in HCC cell models and a xenograft mouse model. The regulatory network between HOTAIR and miR-122 was further detected following overexpression or knockdown of HOTAIR. DNA methylation status of miR-122 promoter region, as well as expression levels of DNMTs, EZH2 and Cyclin G1 were analyzed.
findingsIn this study, we found that HOTAIR was highly expressed whereas miR-122 was suppressed in HCC, and HOTAIR negatively regulated miR-122 expression in HCC cells. Furthermore, knockdown of HOTAIR dramatically inhibited HCC cell proliferation and induced cell cycle arrest in vitro and suppressed tumorigenicity in vivo by upregulating miR-122 expression. Mechanistically, a CpG island was located in the miR-122 promoter region. HOTAIR epigenetically suppressed miR-122 expression via DNMTs-mediated DNA methylation. Moreover, HOTAIR upregulated DNMTs expression via EZH2. In addition, suppression of miR-122 induced by HOTAIR directly reactivated oncogene Cyclin G1 expression. Collectively, our results suggest that HOTAIR epigenetically suppresses miR-122 expression via DNA methylation, leading to activation of Cyclin G1 and promotion of tumorigenicity in HCC, which provide new insight into the mechanism of HOTAIR-mediated hepatocarcinogenesis via suppressing miR-122.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.