ArticlePloS one2024
The promotive role of lncRNA MIR205HG in proliferation, invasion, and migration of melanoma cells via the JMJD2C/ALKBH5 axis.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 6 citations in OpenAlex.
- Mechanism of FOXP2 in the Hepatocellular Carcinoma Progression via Ferroptosis Through RBM15B-Mediated m6A Modification.Applied biochemistry and biotechnology · 2026Article
- LEADR, a p63 target, dampens interferon signalling in bladder cancer.Cell death discovery · 2025Article
- Novel Biological Strategies for Melanoma Therapy: A Focus on lncRNAs and Their Targeting.Cancers · 2025Review
- Molecular Mechanisms and Therapeutic Implications of Long Non-coding RNAs in Cutaneous Biology and Disease.Journal of cellular physiology · 2025Review
- Clarifying new molecular subtyping and precise treatment of melanoma based on disulfidptosis-related lncRNA signature.European journal of medical research · 2024Article
- LncRNAs in melanoma phenotypic plasticity: emerging targets for promising therapies.RNA biology · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma is a highly malignant skin cancer. This study aimed to investigate the role of long non-coding RNA MIR205 host gene (lncRNA MIR205HG) in proliferation, invasion, and migration of melanoma cells via jumonji domain containing 2C (JMJD2C) and ALKB homolog 5 (ALKBH5). Real-time quantitative polymerase chain reaction or Western blot assay showed that MIR205HG, JMJD2C, and ALKBH5 were increased in melanoma cell lines. Cell counting kit-8, colony formation, and Transwell assays showed that silencing MIR205HG inhibited proliferation, invasion, and migration of melanoma cells. RNA immunoprecipitation, actinomycin D treatment, and chromatin immunoprecipitation showed that MIR205HG may bind to human antigen R (HuR, ELAVL1) and stabilized JMJD2C expression, and JMJD2C may increase the enrichment of H3K9me3 in the ALKBH5 promotor region to promote ALKBH5 transcription. The tumor xenograft assay based on subcutaneous injection of sh-MIR205HG-treated melanoma cells showed that silencing MIR205HG suppressed tumor growth and reduced Ki67 positive rate by inactivating the JMJD2C/ALKBH5 axis. Generally, MIR205HG facilitated proliferation, invasion, and migration of melanoma cells through HuR-mediated stabilization of JMJD2C and increasing ALKBH5 transcription by erasing H3K9me3.
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