ArticleBritish journal of cancer2011
Exposure to HIV-protease inhibitors selects for increased expression of P-glycoprotein (ABCB1) in Kaposi's sarcoma cells.
Article in British journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Effect of fentanyl on HIV expression in peripheral blood mononuclear cells.Frontiers in microbiology · 2024Article
- Hepatic Involvement in Acquired Immunodeficiency Syndrome-Associated Kaposi's Sarcoma: A Descriptive Analysis on CT, MRI, and Ultrasound.Infection and drug resistance · 2024Article
- Review
- Targeting the unfolded protein response in head and neck and oral cavity cancers.Experimental cell research · 2019Review
- 'Et tu, inhibitor?': the potential for HIV inhibitors to prime P-gp-mediated chemoresistance in cancer.Future science OA · 2018Article
- Nelfinavir and other protease inhibitors in cancer: mechanisms involved in anticancer activity.F1000Research · 2015Review
- Insights into the broad cellular effects of nelfinavir and the HIV protease inhibitors supporting their role in cancer treatment and prevention.Current opinion in oncology · 2013Review
- Clinical and laboratory characteristics, staging, and outcomes of individuals with AIDS-associated Kaposi's sarcoma at an university hospital.Anais brasileiros de dermatologiaArticle
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundGiven that HIV-protease inhibitors (HIV-PIs) are substrates/inhibitors of the multidrug transporter ABCB1, can induce ABCB1 expression, and are used in combination with doxorubicin for AIDS-Kaposi's Sarcoma (KS) treatment, the role that ABCB1 plays in mediating multidrug resistance (MDR) in a fully transformed KS cell line (SLK) was explored.
methodsThe KS cells were exposed to both acute and chronic treatments of physiological concentrations of different HIV-PIs (indinavir, nelfinavir, atazanavir, ritonavir, or lopinavir), alone or together with doxorubicin. The ABCB1 mRNA and protein expression levels were then assessed by qRT-PCR and western blotting, flow cytometry, and immunofluorescence.
resultsChronic treatment of SLK cells with one of the five HIV-PIs alone or together resulted in increased resistance to doxorubicin. Co-treatment with one of the HIV-PIs in combination with doxorubicin resulted in a synergistic increase in resistance to doxorubicin, and the degree of resistance was found to correlate with the expression of ABCB1. The SLK cells were also revealed to be cross-resistant to the structurally unrelated drug paclitaxel.
conclusionThese studies suggest that ABCB1 is primarily responsible for mediating MDR in SLK cells selected with either HIV-PIs alone or in combination with doxorubicin. Therefore, the roles that ABCB1 and drug cocktails play in mediating MDR in KS in vivo should be evaluated.
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