ArticleCancer letters2014
Carcinogenic metalloid arsenic induces expression of mdig oncogene through JNK and STAT3 activation.
Article in Cancer letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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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Who cites it
33 citing papers in PubMed, 62 citations in OpenAlex.
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- To Erase or Not to Erase: Non-Canonical Catalytic Functions and Non-Catalytic Functions of Members of Histone Lysine Demethylase Families.International journal of molecular sciences · 2024Review
- Epigenetic regulation of breast cancer metastasis.Cancer metastasis reviews · 2024Review
- JMJD family proteins in cancer and inflammation.Signal transduction and targeted therapy · 2022Review
- Depletion ofBiomedicines · 2022Article
- MDIG, a 2‑oxoglutarate‑dependent oxygenase, acts as an oncogene and predicts the prognosis of multiple types of cancer.International journal of oncology · 2022Article
- Arsenic activates STAT3 signaling during the transformation of the human bronchial epithelial cells.Toxicology and applied pharmacology · 2022Article
- 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
- Environmental and Health Hazards of Chromated Copper Arsenate-Treated Wood: A Review.International journal of environmental research and public health · 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
- Environmentally-inducedTheranostics · 2021Article
- TR35 Exerts Anti-tumor Effects by Modulating Mitogen-Activated Protein Kinase and STAT3 Signaling in Lung Cancer Cells.Frontiers in cell and developmental biology · 2021Article
- Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 to Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution.Pharmacological reviews · 2020Review
- The Role of Reactive Oxygen Species in Arsenic Toxicity.Biomolecules · 2020Review
- Mdig promotes oncogenic gene expression through antagonizing repressive histone methylation markers.Theranostics · 2020Article
- New discoveries of mdig in the epigenetic regulation of cancers.Seminars in cancer biology · 2019Review
- EZH2 inhibition suppresses bladder cancer cell growth and metastasis via the JAK2/STAT3 signaling pathway.Oncology letters · 2019Article
- A review of arsenic exposure and lung cancer.Toxicology research · 2019Review
- The emerging roles of ribosomal histidyl hydroxylases in cell biology, physiology and disease.Cellular and molecular life sciences : CMLS · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Environmental or occupational exposure to arsenic, a chemical element classified as metalloid, has been associated with cancer of the lung, skin, bladder, liver, etc. Mdig (mineral dust-induced gene) is a newly identified oncogene linked to occupational lung diseases and lung cancer. It is unclear whether mdig is also involved in arsenic-induced malignant transformation of the lung cells. By using human bronchial epithelial cells and human lung cancer cell lines, we showed that arsenic was able to induce expression of mdig. We further demonstrated that this mdig induction by arsenic was partially dependent on the JNK and STAT3 signaling pathways. Disruption of the JNK or STAT3 by either chemical inhibitors or siRNAs diminished arsenic-induced accumulation of mdig mRNA and protein. Furthermore, we also showed that microRNA-21 (miR-21) and Akt were down-stream effectors of the JNK and STAT3 signaling pathways in arsenic-induced mdig expression. Transfection of the cells with anti-miR-21 or pre-treatment of the cells with Akt inhibitor blunted mdig induction by arsenic. Clinically, the levels of mdig can be applied to predict the disease progression, the first progression (FP), in non-small cell lung cancer (NSCLC) patients. Taken together, our data suggest that mdig may play important roles on the pathogenesis of arsenic-induced lung cancer and that JNK and STAT3 signaling pathways are essential in mediating arsenic-induced mdig expression.
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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.