ArticleInternational journal of molecular sciences2019
Sorafenib-Induced Apoptosis in Hepatocellular Carcinoma Is Reversed by SIRT1.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 82 citations in OpenAlex.
- Comparison of the Effects of Sorafenib and Stem Cell Secretome on HepG2 Cancer Cells with Respect to the Ras/Raf/MEK/ERK Pathway.Journal of clinical medicine · 2026Article
- LncRNA TAF1A-AS1 regulates the progression in hepatocellular carcinoma by targeting miR-664b-3p/USP22 axis.Discover oncology · 2026Article
- Current Therapeutic Strategies, Recent Advances and the Emerging Potential of Natural Products in Hepatocellular Carcinoma.Scientifica · 2026Review
- Post-translational modification in hepatocellular carcinoma resistance: molecular mechanisms and therapeutic targeting.Frontiers in immunology · 2026Review
- Article
- Enhancement of apoptosis in HCT116 and HepG2 cells byChinese herbal medicines · 2025Article
- Fasting in combination with the cocktail Sorafenib:Metformin blunts cellular plasticity and promotes liver cancer cell death via poly-metabolic exhaustion.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- The endoplasmic reticulum degradation-enhancing α-mannosidase-like protein 3 attenuates the unfolded protein response and has pro-survival and pro-viral roles in hepatoma cells and hepatocellular carcinoma patients.Journal of biomedical science · 2025Article
- SIRT1 Inhibition-Induced Mitochondrial Damage Promotes GSDME-Dependent Pyroptosis in Hepatocellular Carcinoma Cells.Molecular biotechnology · 2024Article
- Research advances in the function and anti-aging effects of nicotinamide mononucleotide.Journal of Zhejiang University. Science. B · 2024Review
- Nicotinamide Mononucleotide: Research Process in Cardiovascular Diseases.International journal of molecular sciences · 2024Review
- Ropivacaine synergizes with sorafenib to induce apoptosis of hepatocellular carcinoma cells via the IL-6/STAT3 pathway.Cancer science · 2024Article
- Polydopamine Nanoparticle-Based Combined Chemotherapy and Photothermal Therapy for the Treatment of Liver Cancer.ACS applied materials & interfaces · 2024Article
- Caffeic acid phenethyl ester derivative exerts remarkable anti-hepatocellular carcinoma effect, non-inferior to sorafenib, in vivo analysis.Scientific reports · 2024Article
- Human cytomegalovirus modulates mTORC1 to redirect mRNA translation within quiescently infected monocytes.Journal of virology · 2024Article
- Mechanistic Insights about Sorafenib-, Valproic Acid- and Metformin-Induced Cell Death in Hepatocellular Carcinoma.International journal of molecular sciences · 2024Review
- Ferroptosis and its relationship with cancer.Frontiers in cell and developmental biology · 2024Review
- The Role of Bcl-2 Family Proteins and Sorafenib Resistance in Hepatocellular Carcinoma.International journal of cell biology · 2024Review
- Targeting SIRT1 synergistically improves the antitumor effect of JQ-1 in hepatocellular carcinoma.Heliyon · 2023Article
- Overexpression of miR-4669 Enhances Tumor Aggressiveness and Generates an Immunosuppressive Tumor Microenvironment in Hepatocellular Carcinoma: Its Clinical Value as a Predictive Biomarker.International journal of molecular sciences · 2023Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Sorafenib is a multi-kinase inhibitor and one of the few systemic treatment options for patients with advanced hepatocellular carcinomas (HCCs). Resistance to sorafenib develops frequently and could be mediated by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin (SIRT)1. We aimed to test whether sorafenib efficacy is influenced by cellular NAD levels and NAD-dependent SIRT1 function. We analyzed sorafenib effects on apoptosis induction, NAD salvage, mitochondrial function, and related signaling pathways in HCC cell lines (HepG2, Hep3B, und HUH7) overexpressing SIRT1 or supplemented with the NAD metabolite nicotinamide mononucleotide (NMN) compared to controls. Treatment of HCC cell lines with sorafenib dose-dependently induced apoptosis and a significant decrease in cellular NAD concentrations. The SIRT1 protein was downregulated in HUH7 cells but not in Hep3B cells. After sorafenib treatment, mitochondrial respiration in permeabilized cells was lower, citrate synthase activity was attenuated, and cellular adenosine triphosphate (ATP) levels were decreased. Concomitant to increased phosphorylation of adenosine monophosphate (AMP)-activated protein kinase (AMPK), sorafenib treatment led to decreased activity of the mechanistic target of rapamycin (mTOR), indicative of energy deprivation. Transient overexpression of SIRT1, as well as NAD repletion by NMN, decreased sorafenib-induced apoptosis. We can, therefore, conclude that sorafenib influences the NAD/SIRT1/AMPK axis. Overexpression of SIRT1 could be an underlying mechanism of resistance to sorafenib treatment in HCC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.