ArticleJournal of hematology & oncology2020
MiR-612 regulates invadopodia of hepatocellular carcinoma by HADHA-mediated lipid reprogramming.
Article in Journal of hematology & oncology, 2020. 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 64 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
64 citing papers in PubMed, 108 citations in OpenAlex.
- Glutamine-driven metabolic reprogramming promotes CAR-T cell function through mTOR-SREBP2 mediated HMGCS1 upregulation in ovarian cancer.Journal of translational medicine · 2025Trial
- Inhibition of PI3K/AKT/mTOR pathway suppresses growth of oral squamous cell carcinoma in 2D and 3D in vitro model and animal model.Genes & genomics · 2026Article
- Article
- Melatonin targets mitochondrial trifunctional enzyme HADHA to improve lipid metabolism in metabolic dysfunction-associated steatotic liver disease.Molecular biomedicine · 2026Article
- Cold exposure-inducedActa pharmaceutica Sinica. B · 2026Article
- RORα: a critical nexus in the crosstalk between cholesterol metabolism and macrophage polarization.Frontiers in immunology · 2026Review
- 27-Hydroxycholesterol in cancer development and drug resistance.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Article
- MicroRNA Landscape in Hepatocellular Carcinoma: Metabolic Re-Wiring, Predictive and Diagnostic Biomarkers, and Emerging Therapeutic Targets.Biomedicines · 2025Review
- The functional role of exosomalTranslational cancer research · 2025Article
- The TCF7L2/miR-206/Cofilin1 axis promotes the metastasis of bladder cancer cells by regulating the formation of invadopodia.Acta biochimica et biophysica Sinica · 2025Article
- DLX4 regulates rheumatoid arthritis fibroblast-like synoviocytes invasiveness and a cancer transcriptomic signature.Scientific reports · 2025Article
- Invadopodia in cancer metastasis: dynamics, regulation, and targeted therapies.Journal of translational medicine · 2025Review
- miRNAs-Set of Plasmatic Extracellular Vesicles as Novel Biomarkers for Hepatocellular Carcinoma Diagnosis Across Tumor Stage and Etiologies.International journal of molecular sciences · 2025Article
- MiR-183-5p inhibitor promotes mitoxantrone-induced immunogenic death of hepatoma cells by targeting STC1.International journal of clinical and experimental pathology · 2025Article
- Liquid-liquid phase separation-driven molecular subtyping and prognostic modeling in colorectal cancer.Frontiers in immunology · 2025Article
- Construction of ceRNA networks of lncRNA and miRNA associated with intramuscular fat deposition in Ujumqin sheep.Frontiers in veterinary science · 2025Article
- WTAP-Mediated mJournal of cellular and molecular medicine · 2024Article
- HADHA promotes glioma progression by accelerating MDM2-mediated p53 ubiquitination.Cancer gene therapy · 2024Article
- Research progress in the metabolic reprogramming of hepatocellular carcinoma (Review).Molecular medicine reports · 2024Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNA-612 (miR-612) has been proven to suppress EMT, stemness, and tumor metastasis of hepatocellular carcinoma (HCC) via PI3K/AKT2 and Sp1/Nanog signaling. However, its biological roles on HCC progression are far from elucidated.
methodsWe found direct downstream target of miR-612, hadha by RNA immunoprecipitation and sequencing. To explore its biological characteristic, potential molecular mechanism, and clinical relevance in HCC patients, we performed several in-vitro and in-vivo models, as well as human tissue chip.
resultsEctopic expression of miR-612 could partially reverse the level of HADHA, then suppress function of pseudopods, and diminish metastatic and invasive potential of HCC by lipid reprogramming. In detail, miR-612 might reduce invadopodia formation via HADHA-mediated cell membrane cholesterol alteration and accompanied with the inhibition of Wnt/β-catenin regulated EMT occurrence. Our results showed that the maximum oxygen consumption rates (OCR) of HCCLM3
conclusionmiR-612 can suppress the formation of invadopodia, EMT, and HCC metastasis and by HADHA-mediated lipid programming, which may provide a new insight of miR-612 on tumor metastasis and progression.
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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.