ArticleBioMed research international2019
Dihydroartemisinin Sensitizes Mutant p53 (R248Q)-Expressing Hepatocellular Carcinoma Cells to Doxorubicin by Inhibiting P-gp Expression.
Article in BioMed research international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 72 citations in OpenAlex.
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- Characterization of chemoresistant human non-small cell lung cancer cells by metabolic and lipidomic profiling.Metabolomics : Official journal of the Metabolomic Society · 2023Article
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- Roles of conventional and complementary therapies in recurrent hepatocellular carcinoma.World journal of gastrointestinal oncology · 2023Review
- Frontier progress of the combination of modern medicine and traditional Chinese medicine in the treatment of hepatocellular carcinoma.Chinese medicine · 2022Review
- Development of nanoscale drug delivery systems of dihydroartemisinin for cancer therapy: A review.Asian journal of pharmaceutical sciences · 2022Review
- Genus Sophora: a comprehensive review on secondary chemical metabolites and their biological aspects from past achievements to future perspectives.Archives of pharmacal research · 2021Review
- Anti-malarial drug: the emerging role of artemisinin and its derivatives in liver disease treatment.Chinese medicine · 2021Review
- Dihydroartemisinin as a Sensitizing Agent in Cancer Therapies.OncoTargets and therapy · 2021Review
- Repurposing Artemisinin and its Derivatives as Anticancer Drugs: A Chance or Challenge?Frontiers in pharmacology · 2021Review
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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
Mutant p53 (R248Q) induces doxorubicin (ADM) resistance in hepatocellular carcinoma (HCC). Dihydroartemisinin (DHA) can synergistically enhance anticancer effect of many chemotherapeutic agents. However, whether DHA could increase therapeutic efficacy of ADM in p53 (R248Q)-expressing HCC cells remains unknown. In the present study, we established mutant p53 (R248Q)-expressing Hep3B cells to study the effect and mechanism of DHA on ADM resistance and the synergistic effect of DHA with ADM. We found that P-gp was highly expressed in p53 (R248Q)-expressing Hep3B cells. As a result, cells expressing p53 (R248Q) displayed higher cell viability and lower cell apoptosis level upon ADM treatment. Meanwhile, phosphorylation levels of ERK1/2 and p65 were elevated in p53 (R248Q)-expressing Hep3B cells. However, combination of DHA and ADM treatment decreased cell viability and elevated cell apoptosis level in p53 (R248Q)-expressing Hep3B cells. Molecular dynamics simulations showed that DHA had the potential to bind with mutant p53 (R248Q) protein. Furthermore, DHA treatment decreased P-gp expression and inhibited phosphorylation levels of ERK1/2 and p65 in p53 (R248Q)-expressing Hep3B cells. Finally, DHA treatment could significantly reduce ADM efflux in p53 (R248Q)-expressing cells. Our results indicate that DHA could decrease P-gp expression via inhibiting the p53 (R248Q)-ERK1/2-NF-
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