ArticleScientific reports2018
Sodium orthovanadate overcomes sorafenib resistance of hepatocellular carcinoma cells by inhibiting Na
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Chemotaxis of ATPase-Powered Nanoparticles up Extra- and Intracellular ATP Gradients.Nano letters · 2026Article
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- Exploring the potential mechanisms of sorafenib resistance in hepatocellular carcinoma cell lines based on RNA sequencing.Cancer cell international · 2025Article
- Potassium channels as novel molecular targets in hepatocellular carcinoma (Review).Oncology reports · 2023Review
- Coleon U, Isolated fromPharmaceutics · 2023Article
- Nalidixic acid potentiates the antitumor activity in sorafenib-resistant hepatocellular carcinomaFrontiers in pharmacology · 2022Article
- Link of sorafenib resistance with the tumor microenvironment in hepatocellular carcinoma: Mechanistic insights.Frontiers in pharmacology · 2022Review
- Phosphatase inhibition by sodium orthovanadate displays anti-inflammatory action by suppressing AKT-IKKβ signaling in RAW264.7 cells.Toxicology reports · 2022Article
- Effect of the Hypoxia Inducible Factor on Sorafenib Resistance of Hepatocellular Carcinoma.Frontiers in oncology · 2021Review
- Hypoxia induces sorafenib resistance mediated by autophagy via activating FOXO3a in hepatocellular carcinoma.Cell death & disease · 2020Article
- Role of Impaired Nutrient and Oxygen Deprivation Signaling and Deficient Autophagic Flux in Diabetic CKD Development: Implications for Understanding the Effects of Sodium-Glucose Cotransporter 2-Inhibitors.Journal of the American Society of Nephrology : JASN · 2020Review
- Article
- Sodium homeostasis in the tumour microenvironment.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- LncRNA SNHG1 contributes to sorafenib resistance by activating the Akt pathway and is positively regulated by miR-21 in hepatocellular carcinoma cells.Journal of experimental & clinical cancer research : CR · 2019Article
- TINAGL1 promotes hepatocellular carcinogenesis through the activation of TGF-β signaling-medicated VEGF expression.Cancer management and research · 2019Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The resistance to sorafenib highly affects its clinical benefits for treating hepatocellular carcinoma (HCC). Sodium orthovanadate (SOV) is a phosphate analog that displays anti-cancer activities against various types of malignancies including HCC. The present study has demonstrated that SOV is able to overcome sorafenib resistance and strengthens sorafenib in suppressing sorafenib-resistant HCC cells in vitro and in animal models. Similar to its action on parental HCC cells, SOV induced cell cycle arrest at G2/M phases by regulating cyclin B1 and cyclin-dependent kinase 1, and apoptosis by reducing mitochondrial membrane potential, in sorafenib-resistant HCC cells. More importantly, SOV inhibited ATPase activity, which was significantly elevated in sorafenib-resistant HCC cells. SOV also reduced the expression of HIF-1α and HIF-2α and their nuclear translocation, resulting in downregulation of their downstream factors including vascular endothelial growth factor, lactate dehydrogenase-A and glucose transporter 1. Its ability to inhibit ATPase activity and hypoxia-inducible pathways enabled SOV to efficiently suppress both normoxic and hypoxic cells, which compose cancer cell populations inside sorafenib-resistant HCC tumors. The present results indicate that SOV may be a potent candidate drug for overcoming the resistance to sorafenib in treating HCC.
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