ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
Arsenic trioxide potentiates the anti-cancer activities of sorafenib against hepatocellular carcinoma by inhibiting Akt activation.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- The Role of Bcl-2 Family Proteins and Sorafenib Resistance in Hepatocellular Carcinoma.International journal of cell biology · 2024Review
- Paradoxical effects of arsenic in the lungs.Environmental health and preventive medicine · 2021Review
- SilencingAging · 2020Article
- Combinatorial Low Dose Arsenic Trioxide and Cisplatin Exacerbates Autophagy via AMPK/STAT3 Signaling on Targeting Head and Neck Cancer Initiating Cells.Frontiers in oncology · 2020Article
- Arsenic trioxide-induced upregulation of miR-1294 suppresses tumor growth in hepatocellular carcinoma by targeting TEAD1 and PIM1.Cancer biomarkers : section A of Disease markers · 2020Article
- Is the era of sorafenib over? A review of the literature.Therapeutic advances in medical oncology · 2020Review
- Therapeutic effect and adverse reaction of sorafenib in the treatment of advanced renal cancer.Oncology letters · 2019Article
- Arsenic trioxide reverses the chemoresistance in hepatocellular carcinoma: a targeted intervention of 14-3-3η/NF-κB feedback loop.Journal of experimental & clinical cancer research : CR · 2018Article
- Arsenic trioxide and sorafenib combination therapy for human hepatocellular carcinoma functions via up-regulation of TNF-related apoptosis-inducing ligand.Oncology letters · 2018Article
- Enhanced antitumor activity of combined megestrol acetate and arsenic trioxide treatment in liver cancer cells.Experimental and therapeutic medicine · 2018Article
- The synergistic antitumor effect of arsenic trioxide combined with cytotoxic T cells in pulmonary metastasis model of colon cancer.Oncotarget · 2017Article
- Melatonin enhances sorafenib actions in human hepatocarcinoma cells by inhibiting mTORC1/p70S6K/HIF-1α and hypoxia-mediated mitophagy.Oncotarget · 2017Article
- Article
- Therapeutic Potential of Arsenic Trioxide (ATO) in Treatment of Hepatocellular Carcinoma: Role of Oxidative Stress in ATO-Induced Apoptosis.Annals of clinical pathology · 2017Article
- Systematic dissection of dysregulated transcription factor-miRNA feed-forward loops across tumor types.Briefings in bioinformatics · 2016Article
- Arsenic trioxide inhibits lung metastasis of mouse colon cancer via reducing the infiltration of regulatory T cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Endothelial to mesenchymal transition contributes to arsenic-trioxide-induced cardiac fibrosis.Scientific reports · 2016Article
- Akt activation correlates with the tumor aggressiveness in Tunisian patients with bladder cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Smad3 Sensitizes Hepatocelluar Carcinoma Cells to Cisplatin by Repressing Phosphorylation of AKT.International journal of molecular sciences · 2016Article
- Modulation of Autophagy by Sorafenib: Effects on Treatment Response.Frontiers in pharmacology · 2016Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sorafenib is the standard first-line systemic drug for advanced hepatocellular carcinoma (HCC), but it also induces the activation of Akt, which contributes to the mechanisms for the resistance to sorafenib. Arsenic trioxide (ATO) is a currently clinically used anticancer drug and displays its anticancer activities by inhibiting Akt activation. Therefore, we hypothesized that ATO may potentiate the anti-cancer activities of sorafenib against HCC. The results have demonstrated that ATO synergized with sorafenib to inhibit the proliferation and promote the apoptosis of HCC cells by diminishing the increased activation of Akt by sorafenib. ATO was shown to inhibit the expression or activation of Akt downstream factors, including glycogen synthase kinase (GSK)-3β, mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (S6K), and eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1), which regulate cell apoptosis and were upregulated or activated by sorafenib. Both sorafenib and ATO downregulated the expression of cyclin D1, resulting in HCC cells arrested at G0/G1 phase. ATO downregulated the expression of Bcl-2 and Bcl-xL and upregulated the expression of Bax, indicating that ATO could induce the apoptosis of HCC cells through the intrinsic pathways; but sorafenib showed little effects on these proteins of Bcl-2 family. ATO synergized with sorafenib to suppress the growth of HCC tumors established in mice by inhibiting the proliferation and inducing the apoptosis of HCC cells in situ. These results indicate that ATO may be a potential agent that given in combination with sorafenib acts synergistically for treating HCC.
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