ArticleOncology letters2015
Targeting hypoxia-inducible factor-2α enhances sorafenib antitumor activity via β-catenin/C-Myc-dependent pathways in hepatocellular carcinoma.
Article in Oncology letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Mechanisms of drug resistance in hepatocellular carcinoma.Biological procedures online · 2025Review
- Review
- Inhibition of EGFR Overcomes Acquired Lenvatinib Resistance Driven by STAT3-ABCB1 Signaling in Hepatocellular Carcinoma.Cancer research · 2022Article
- Link of sorafenib resistance with the tumor microenvironment in hepatocellular carcinoma: Mechanistic insights.Frontiers in pharmacology · 2022Review
- Effect of the Hypoxia Inducible Factor on Sorafenib Resistance of Hepatocellular Carcinoma.Frontiers in oncology · 2021Review
- Review
- Review
- The mechanisms of sorafenib resistance in hepatocellular carcinoma: theoretical basis and therapeutic aspects.Signal transduction and targeted therapy · 2020Review
- Hypoxia-Induced Aquaporin-3 Changes Hepatocellular Carcinoma Cell Sensitivity to Sorafenib by Activating the PI3K/Akt Signaling Pathway.Cancer management and research · 2020Article
- Article
- Cyclin-dependent kinase inhibitor 2B gene is associated with the sensitivity of hepatoma cells to Sorafenib.OncoTargets and therapy · 2019Article
- Sorafenib resistance in hepatocarcinoma: role of hypoxia-inducible factors.Experimental & molecular medicine · 2018Review
- Identification of WT1 as determinant of heptatocellular carcinoma and its inhibition by Chinese herbal medicineOncotarget · 2017Article
- Hypoxia inducible factors in hepatocellular carcinoma.Oncotarget · 2017Review
- Article
- Enhanced angiogenesis, hypoxia and neutrophil recruitment during Myc-induced liver tumorigenesis in zebrafish.Scientific reports · 2016Article
- Epigenetic Activation of Wnt/β-Catenin Signaling in NAFLD-Associated Hepatocarcinogenesis.Cancers · 2016Review
- The prognostic role of lactate dehydrogenase serum levels in patients with hepatocellular carcinoma who are treated with sorafenib: the influence of liver fibrosis.Journal of gastrointestinal oncology · 2016Article
- Hypoxia-inducible factors as molecular targets for liver diseases.Journal of molecular medicine (Berlin, Germany) · 2016Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sorafenib is a type of multikinase inhibitor that exhibits antiangiogenic and antiproliferative effects; in addition, sorafenib is a unique first-line drug recommended for the treatment of advanced hepatocellular carcinoma (HCC). However, the effectiveness of HCC treatment remains poor due to acquired drug resistance. It has been suggested that hypoxia, induced as a results of the antiangiogenic effects of sustained sorafenib treatment, may be an important factor in sorafenib resistance. The transcription factor hypoxia-inducible factor (HIF)-2α has been reported to be associated with cell proliferation under hypoxic conditions; therefore, it was hypothesized that hypoxia may enhance tumor cell proliferation via this mechanism. The present study aimed to evaluate whether the knock-down of HIF-2α was able to enhance the therapeutic efficacy of sorafenib in order to effectively treat HCC. The results demonstrated that hypoxia protected HCC cells against sorafenib; however, short hairpin RNA-HIF-2α transfection in combination with sorafenib treatment exhibited a significantly synergistic effect against HCC cell proliferation. In addition, HCC cells acquired increased β-catenin/C-Myc expression, which enhanced proliferation under hypoxic conditions; however, targeted knock-down of HIF-2α or C-Myc markedly decreased cell proliferation in HCC cells. In conclusion, the results of the present study indicated that the targeted knock-down of HIF-2α in combination with sorafenib may be a promising strategy for the treatment of HCC.
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