Pentagalloyl Glucose-Targeted Inhibition of P-Glycoprotein and Re-Sensitization of Multidrug-Resistant Leukemic Cells (K562/ADR) to Doxorubicin: In Silico and Functional Studies.
Nathupakorn DechsupaNopawit KhamtoPornthip ChawapunSadanon SiriphongPhattarawadee InnuanAuthaphinya SuwanThitiworada LuangsuepNichakorn PhotilimthanaWitchayaporn MaitaRossarin ThanacharttanatchayaPadchanee SangthongPuttinan MeepowpanChatchanok UdomtanakunchaiJiraporn KantapanPublished in: Pharmaceuticals (Basel, Switzerland) (2023)
Combining phytochemicals with chemotherapeutic drugs has demonstrated the potential to surmount drug resistance. In this paper, we explore the efficacy of pentagalloyl glucose (PGG) in modulating P-gp and reversing multidrug resistance (MDR) in drug-resistant leukemic cells (K562/ADR). The cytotoxicity of PGG was evaluated using a CCK-8 assay, and cell apoptosis was assessed using flow cytometry. Western blotting was used to analyze protein expression levels. P-glycoprotein (P-gp) activity was evaluated by monitoring the kinetics of P-gp-mediated efflux of pirarubicin (THP). Finally, molecular docking, molecular dynamics simulation, and molecular mechanics with generalized Born and surface area solvation (MM-GBSA) calculation were conducted to investigate drug-protein interactions. We found that PGG selectively induced cytotoxicity in K562/ADR cells and enhanced sensitivity to doxorubicin (DOX), indicating its potential as a reversal agent. PGG reduced the expression of P-gp and its gene transcript levels. Additionally, PGG inhibited P-gp-mediated efflux and increased intracellular drug accumulation in drug-resistant cells. Molecular dynamics simulations and MM-GBSA calculation provided insights into the binding affinity of PGG to P-gp, suggesting that PGG binds tightly to both the substrate and the ATP binding sites of P-gp. These findings support the potential of PGG to target P-gp, reverse drug resistance, and enhance the efficacy of anticancer therapies.
Keyphrases
- molecular dynamics simulations
- drug resistant
- multidrug resistant
- molecular docking
- induced apoptosis
- cell cycle arrest
- acinetobacter baumannii
- signaling pathway
- endoplasmic reticulum stress
- gene expression
- type diabetes
- poor prognosis
- oxidative stress
- cell death
- acute myeloid leukemia
- preterm infants
- cystic fibrosis
- metabolic syndrome
- amino acid
- risk assessment
- pseudomonas aeruginosa
- transcription factor
- rna seq
- south africa
- endothelial cells
- human health