ArticleJournal of experimental & clinical cancer research : CR2020
Loss of miR-192-5p initiates a hyperglycolysis and stemness positive feedback in hepatocellular carcinoma.
Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Review
- Understanding how hypoxia contributes to liver cancer stem cells maintenance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Investigating the association of NBN gene polymorphisms with multiple cancers through statistical meta-analysis and bioinformatics insights.Biology methods & protocols · 2026Review
- MicroRNA Landscape in Hepatocellular Carcinoma: Metabolic Re-Wiring, Predictive and Diagnostic Biomarkers, and Emerging Therapeutic Targets.Biomedicines · 2025Review
- Molecular mechanisms of miR-192 in cancer: a biomarker and therapeutic target.Cancer cell international · 2025Review
- Liver-specific gene PGRMC1 blocks c-Myc-induced hepatocarcinogenesis through ER stress-independent PERK activation.Nature communications · 2025Article
- The role of liver cancer stem cells in hepatocellular carcinoma metastasis.Cancer biology & therapy · 2024Review
- Little things with significant impact: miRNAs in hepatocellular carcinoma.Frontiers in oncology · 2023Review
- The role of PFKFB3 in maintaining colorectal cancer cell proliferation and stemness.Molecular biology reports · 2022Review
- Article
- miR-3682-3p directly targets FOXO3 and stimulates tumor stemness in hepatocellular carcinomaWorld journal of stem cells · 2022Article
- RacGAP1 promotes the malignant progression of cervical cancer by regulating AP-1 via miR-192 and p-JNK.Cell death & disease · 2022Article
- LncRNA CARMN Affects Hepatocellular Carcinoma Prognosis by Regulating the miR-192-5p/LOXL2 Axis.Oxidative medicine and cellular longevity · 2022Article
- Cancer stem cells: advances in biology and clinical translation-a Keystone Symposia report.Annals of the New York Academy of Sciences · 2021Review
- Long Non-Coding RNA LINC01572 Promotes Hepatocellular Carcinoma ProgressionFrontiers in cell and developmental biology · 2021Article
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Authors and funding
14 authors at 5 institutions in 4 countries.
Funding
Abstract
backgroundEmerging studies revealed that cancer stem cells (CSCs) possessed peculiar metabolic properties, which however remained largely unknown in hepatocellular carcinoma (HCC). Genetic silencing of liver-abundant miR-192-5p was a key feature for multiple groups of CSC-positive HCCs. We thus aimed to investigate essential metabolic features of hepatic CSCs via using HCCs with miR-192-5p silencing as a model.
methodsDatasets from two independent HCC cohorts were used. Data integration analyses of miR-192-5p with metabolome and mRNA transcriptome data in HCC Cohort 1 were performed to investigate miR-192-5p related metabolic features, which was further validated in Cohort 2. Cellular and molecular assays were performed to examine whether and how miR-192-5p regulated the identified metabolic features. Co-culture systems consisting of HCC cells and LX2 (human hepatic stellate cell line) or THP1 (human monocyte cell line) were established to explore effects of the identified metabolic properties on stemness features of HCC cells via interacting with co-cultured non-tumor cells.
resultsHigh levels of glycolysis-related metabolites and genes were present in HCCs with low miR-192-5p and CSC-positive HCCs in two independent HCC cohorts. miR-192-5p knockout cells displayed CSC features and miR-192-5p loss led to an enhanced glycolytic phenotype via upregulating three bona fide targets, GLUT1 and PFKFB3 (two glycolytic enzymes) and c-Myc (regulating glycolytic genes' expression). Meanwhile, c-Myc suppressed miR-192-5p transcription, ensuring a low-miR-192-5p/high-c-Myc loop to maintain hyperglycolysis. Moreover, over-produced lactic acid from hyperglycolytic HCC cells stimulated the ERK phosphorylation of co-cultured LX2 and THP1 non-tumor cells partially via NDRG3 and MCT1, which in turn promoted cell malignancy and stemness of HCC cells. Consistently, HCC patients with low level of miR-192-5p in their tumor tissues and high level of NDRG3 or MCT1 in their non-tumor tissues had the shortest overall survival.
conclusionsIn CSC-positive HCCs, miR-192-5p loss enhanced glycolysis and over produced lactate might further increase HCC malignant features via interacting with environmental non-tumor cells.
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