ArticleOncotarget2013
Mdig de-represses H19 large intergenic non-coding RNA (lincRNA) by down-regulating H3K9me3 and heterochromatin.
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 81 citations in OpenAlex.
- Functional role of long non-coding RNA MALAT1 and HOTAIR in lung cancer.Non-coding RNA research · 2026Review
- Long noncoding RNAs at the crossroads of smoking, oxidative stress, inflammation, and lung disease.Archives of toxicology · 2026Review
- Mina53 demethylates histone H4 arginine 3 asymmetric dimethylation to regulate neural stem/progenitor cell identity.Nature communications · 2024Article
- Epigenetic regulation of breast cancer metastasis.Cancer metastasis reviews · 2024Review
- Long non-coding RNA H19: a potential biomarker and therapeutic target in human malignant tumors.Clinical and experimental medicine · 2023Review
- Epigenetics and environment in breast cancer: New paradigms for anti-cancer therapies.Frontiers in oncology · 2022Review
- Cooperation between NRF2-mediated transcription and MDIG-dependent epigenetic modifications in arsenic-induced carcinogenesis and cancer stem cells.Seminars in cancer biology · 2021Review
- Pathological and Prognostic Indications of the mdig Gene in Human Lung Cancer.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Article
- Cancer Susceptibility Candidate 9 (CASC9): A Novel Targetable Long Noncoding RNA in Cancer Treatment.Translational oncology · 2020Review
- CRISPR-Cas9 gene editing causes alternative splicing of the targeting mRNA.Biochemical and biophysical research communications · 2020Article
- Exosomal Long Non-Coding RNAs in Lung Diseases.International journal of molecular sciences · 2020Review
- Molecular Signatures ofCancers · 2020Article
- Long Non-Coding RNAs in Biliary Tract Cancer-An Up-to-Date Review.Journal of clinical medicine · 2020Review
- Mdig promotes oncogenic gene expression through antagonizing repressive histone methylation markers.Theranostics · 2020Article
- The Roles of H19 in Regulating Inflammation and Aging.Frontiers in immunology · 2020Review
- Noncoding RNAs and Liquid Biopsy in Lung Cancer: A Literature Review.Diagnostics (Basel, Switzerland) · 2019Review
- Long non-coding RNAs in non-small cell lung cancer: functions and distinctions from other malignancies.Translational cancer research · 2019Review
- MDIG promotes cisplatin resistance of lung adenocarcinoma by regulating ABC transporter expression via activation of the WNT/β-catenin signaling pathway.Oncology letters · 2019Article
- Long non‑coding RNAs in lung cancer: Regulation patterns, biologic function and diagnosis implications (Review).International journal of oncology · 2019Review
- New discoveries of mdig in the epigenetic regulation of cancers.Seminars in cancer biology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Mineral dust-induced gene (mdig) had been linked to the development of human lung cancers associated with environmental exposure to mineral dust, tobacco smoke or other carcinogens. In the present studies, we demonstrated that the overexpression of mdig in A549 adenocarcinomic human alveolar type II epithelial cells decreases the heterochromatin conformation of the cells and de-represses the transcription of genes in the tandemly repeated DNA regions. Although mdig can only cause a marginal decrease of the total histone H3 lysine 9 trimethylation (H3K9me3), a significant reduction of H3K9me3 in the promoter region of H19, the paternally imprinted but maternally expressed gene transcribing a large intergenic non-coding RNA (lincRNA), was observed in the cells with mdig overexpression. Silencing mdig by either shRNA or siRNA not only increased the level of H3K9me3 in the promoter region of H19 but also attenuated the transcription of H19 long non-coding RNA. Demethylation assays using immunoprecipitated mdig and histone H3 peptide substrate suggested that mdig is able to remove the methyl groups from H3K9me3. Clinically, we found that higher levels of mdig and H19 expression correlate with poorer survival of the lung cancer patients. Taken together, our results imply that mdig is involved in the regulation of H3K9me3 to influence the heterochromatin structure of the genome and the expression of genes important for cell growth or transformation.
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Registered trials
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.