ArticleOncogene2021
Cytochrome P450 1A2 overcomes nuclear factor kappa B-mediated sorafenib resistance in hepatocellular carcinoma.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Multi-omics analysis of key lipid metabolism-related genes involved in the anti-hepatocellular carcinoma effect of dihydroartemisinin.Discover oncology · 2026Article
- Therapeutic potential of natural triterpenoids in liver cancer.Medical oncology (Northwood, London, England) · 2025Review
- Identification of potential biomarkers for breast cancer based on salivary metabolomics.Frontiers in oncology · 2025Article
- Decoding the Role of CYP450 Enzymes in Metabolism and Disease: A Comprehensive Review.Biomedicines · 2024Review
- CREB3 facilitates Donafenib resistance in hepatocellular carcinoma cells via the LSD1/CoREST/p65 axis by transcriptionally activating long noncoding RNA ZFAS1.Translational oncology · 2024Article
- DEAD-Box Helicase 17 exacerbates non-alcoholic steatohepatitis via transcriptional repression of cyp2c29, inducing hepatic lipid metabolism disorder and eliciting the activation of M1 macrophages.Clinical and translational medicine · 2024Article
- Article
- Advances in hepatocellular carcinoma drug resistance models.Frontiers in medicine · 2024Review
- Novel roles of PIWI proteins and PIWI-interacting RNAs in human health and diseases.Cell communication and signaling : CCS · 2023Review
- Circular RNAs in hepatocellular carcinoma: Recent advances.World journal of gastrointestinal oncology · 2022Review
- Effects of Sensitized Sorafenib with a Paeoniflorin and Geniposide Mixture on Liver Cancer via the NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Article
- Hepatic Cancer Stem Cells: Molecular Mechanisms, Therapeutic Implications, and Circulating Biomarkers.Cancers · 2021Review
- Article
- Oncolytic Viruses in Combination Therapeutic Approaches with Epigenetic Modulators: Past, Present, and Future Perspectives.Cancers · 2021Review
- Article
- The Crosstalk Between Regulatory Non-Coding RNAs and Nuclear Factor Kappa B in Hepatocellular Carcinoma.Frontiers in oncology · 2021Review
- Synthesis, characterization, and antiproliferative evaluation of novel sorafenib analogs for the treatment of hepatocellular carcinoma.Journal of advanced pharmaceutical technology & researchArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sorafenib resistance has become the main obstacle in the effective treatment of advanced hepatocellular carcinoma (HCC) patients. Activation of nuclear factor kappa B (NF-κB) is a newly identified mechanism that contributes to desensitized sorafenib. Cytochrome P450 1A2 (CYP1A2) functions as a tumor suppressor in HCC and its expression is negatively associated with NF-κB in the liver. This study aimed to study whether CYP1A2 could overcome sorafenib resistance. To investigate whether CYP1A2 and NF-κB p65 played roles in sorafenib desensitization, we established sorafenib-resistant (SR) HCC cells. SR cells decreased the expression of CYP1A2 along with the upregulation of NF-κB p65. CYP1A2 overexpression attenuated SR cell proliferation, increased sorafenib sensitivity, and inhibited the NF-κB pathway, whereas CYP1A2 silence showed opposite effects. Sorafenib, in combination with omeprazole, a CYP1A2 inducer, significantly hindered the growth and invasion of SR cells in vitro as well as decreased the tumor growth in vivo. The combination treatment markedly increased CYP1A2 expression and inhibited the sorafenib-induced NF-κB signaling. In addition, the overexpression of NF-κB p65 stimulated the SR cell growth and desensitized sorafenib in SR cells, where CYP1A2 overexpression reversed the phenomenon. Lastly, the majority of HCC tissue samples displayed decreased CYP1A2 but increased NF-κB p65 protein expression. Collectively, CYP1A2 can sensitize SR cells to sorafenib via inhibiting NF-κB p65 axis. Omeprazole in combination with sorafenib exerts a synergistic effect in alleviating acquired sorafenib resistance.
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