ArticleJournal of experimental & clinical cancer research : CR2025
MiR-423-5p is a metabolic and growth tuner in hepatocellular carcinoma via MALAT-1 and mitochondrial interaction.
Article in Journal of experimental & clinical cancer research : CR, 2025. 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 5 papers, 1 of them a synthesis that pooled it.
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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
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Non-coding RNAs and Mitochondrial Dysfunction in Alzheimer's Disease: A Systematic Review.Molecular neurobiology · 2026Pooled it
- miRNA-lncRNA Cross-Regulation Landscape in Cancer: From Molecular Mechanisms to Therapeutic and Diagnostic Applications.Cancers · 2026Review
- The lncRNA-DNA Methylation Axis in Hepatocellular Carcinoma: Mechanisms, Epigenetic Plasticity, and Biological Implications.Biology · 2026Review
- Correction: MiR-423-5p is a metabolic and growth tuner in hepatocellular carcinoma via MALAT-1 and mitochondrial interaction.Journal of experimental & clinical cancer research : CR · 2025Article
- Proteomic profiling identifies miR-423-5p as a modulator of oncogenic metabolism in HCC.Journal of translational medicine · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are key regulators of gene expression and play a crucial role in cancer progression. Recent studies have highlighted miR-423-5p as a potential modulator in hepatocellular carcinoma (HCC), especially in patients responding to sorafenib treatment. A functional interaction with the oncogenic lncRNA MALAT-1 has been hypothesized, suggesting a regulatory mechanism that may influence tumor aggressiveness.
methodsTo investigate this interaction, we analyzed in silico patient datasets to correlate miR-423-5p and MALAT-1 expression with overall survival (OS) and disease free survival (DFS). Stable overexpression of miR-423-5p and MALAT-1 was achieved in HCC cell lines (HepG2, Hep3B, and SNU387) using a lentiviral transduction system. Functional assays were performed to assess proliferation, migration, invasion, and clonogenic potential. The interaction between miR-423-5p and MALAT-1 was confirmed by RNA immunoprecipitation (RIP), followed by transcriptomic analysis using next-generation sequencing (NGS). Mitochondrial activity was evaluated using the Seahorse Mito Stress Test to measure oxygen consumption rate (OCR) and ATP production. In vivo experiments in orthotopic mouse models were performed to assess tumor growth.
resultsPatient data analysis revealed that high miR-423-5p expression correlated with a less aggressive tumor phenotype and improved survival, while MALAT-1 was associated with poorer prognosis. In vitro, miR-423-5p overexpression reduced MALAT-1 levels and significantly impaired proliferation, migration, and invasion. NGS analysis identified transcriptomic changes linked to tumor progression and metabolic shift. The Seahorse Mito Stress Test demonstrated decreased cellular respiration and ATP production upon miR-423-5p overexpression. In vivo, both tumors derived from miR-423-5p-overexpressing cells and MALAT-1 downregulation by ASO GapmeR evidenced a significantly reduced growth compared to controls.
conclusionThese findings suggest, for the first time, that miR-423-5p acts as a tumor suppressor affecting mitochondrial metabolism through MALAT-1 downregulation in HCC. This regulatory axis represents a potential therapeutic target for precision medicine approaches in liver cancer.
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