ArticleScientific reports2021
High glucose induced c-Met activation promotes aggressive phenotype and regulates expression of glucose metabolism genes in HCC cells.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.
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Who cites it
14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 19 citations in OpenAlex.
- Recent Advancements in Known and Emerging Risk Factors of Hepatocellular Carcinoma.Cancer medicine · 2025Pooled it
- Metabolic reprogramming in hepatocellular carcinoma: a bibliometric and visualized study from 2011 to 2023.Frontiers in pharmacology · 2024Pooled it
- Monocyte Preprogramming by Tobacco Carcinogens and Fructose Intake Accelerates Lung Cancer Progression via Metabolic and Epigenetic Pathways.International journal of biological sciences · 2026Article
- Establishment and characterization of a novel imatinib-resistant dermatofibrosarcoma protuberans cell line, DFSP-DPH1.Human cell · 2025Article
- High glucose facilitates hepatocellular carcinoma cell proliferation and invasion via WTAP-mediated HK2 mRNA stability.Molecular and cellular biochemistry · 2025Article
- Metabolic reprogramming of glucose: the metabolic basis for the occurrence and development of hepatocellular carcinoma.Frontiers in oncology · 2025Review
- Review
- High glucose inhibits autophagy and promotes the proliferation and metastasis of colorectal cancer through the PI3K/AKT/mTOR pathway.Cancer medicine · 2024Article
- CAR-T cell therapy for hepatocellular carcinoma: current trends and challenges.Frontiers in immunology · 2024Review
- The Role of Type 2 Diabetes Mellitus-Related Risk Factors and Drugs in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2024Review
- High glucose-induced NCAPD2 upregulation promotes malignant phenotypes and regulates EMT via the Wnt/β-catenin signaling pathway in HCC.American journal of cancer research · 2024Article
- B cell linker protein (BLNK) is a regulator of Met receptor signaling and trafficking in non-small cell lung cancer.iScience · 2022Article
- High glucose causes developmental abnormalities in neuroepithelial cysts with actin and HK1 distribution changes.Frontiers in cell and developmental biology · 2022Article
- Hyperglycemia AltersIn vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is strongly associated with metabolic dysregulations/deregulations and hyperglycemia is a common metabolic disturbance in metabolic diseases. Hyperglycemia is defined to promote epithelial to mesenchymal transition (EMT) of cancer cells in various cancers but its molecular contribution to HCC progression and aggressiveness is relatively unclear. In this study, we analyzed the molecular mechanisms behind the hyperglycemia-induced EMT in HCC cell lines. Here, we report that high glucose promotes EMT through activating c-Met receptor tyrosine kinase via promoting its ligand-independent homodimerization. c-Met activation is critical for high glucose induced acquisition of mesenchymal phenotype, survival under high glucose stress and reprogramming of cellular metabolism by modulating glucose metabolism gene expression to promote aggressiveness in HCC cells. The crucial role of c-Met in high glucose induced EMT and aggressiveness may be the potential link between metabolic syndrome-related hepatocarcinogenesis and/or HCC progression. Considering c-Met inhibition in hyperglycemic patients would be an important complementary strategy for therapy that favors sensitization of HCC cells to therapeutics.
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