Indeed, many genes, including genes encoding drug transporters (ABCB1), drug targets (SCN1A), drug-metabolizing enzymes (CYP2C9, CYP2C19), and human leucocyte antigen (HLA) proteins, may regulate the mechanisms of drug resistance in epilepsy.
This study investigates the effect of the Pgp inhibitor verapamil on the anticonvulsant effect of CBZ and its nanoparticulate formulation in the rat model of isoniazid-induced epilepsy.
These data indicate that the miR-338-5p/EGFR/ABCB1 regulatory loop plays a critical role in HCC, and a negative correlation between miR-338-5p and EGFR or ABCB1 was also detected in HCC clinical samples.
We tested whether the uremic toxin indoxyl sulfate (IS), an endogenous ligand of the transcription factor aryl hydrocarbon receptor, could change the expression of the following liver transporters involved in drug clearance: <i>SLC10A1</i>, <i>SLC22A1</i>, <i>SLC22A7</i>, <i>SLC47A1</i>, <i>SLCO1B1</i>, <i>SLCO1B3</i>, <i>SLCO2B1</i>, <i>ABCB1</i>, <i>ABCB11</i>, <i>ABCC2</i>, <i>ABCC3</i>, <i>ABCC4</i>, <i>ABCC6</i>, and <i>ABCG2</i> We showed that IS increases the expression and activity of the efflux transporter P-glycoprotein (P-gp) encoded by <i>ABCB1</i> in human hepatoma cells (HepG2) without modifying the expression of the other transporters.
P-glycoprotein or membrane pump induced drug efflux and altered prosurvival Bcl-2 expression are key mechanisms for drug resistance leading to failure of chemotherapy in HCC.
Using in vitro assays, we show that repeated miRNA treatments resulted in gradual reduction of HCC cell proliferation and reversal of doxorubicin resistance.
DTA0100 mitotic arrest properties were investigated in two multi-drug resistant cancer cell lines with P-glycoprotein overexpression (colorectal carcinoma and glioblastoma).
This study aimed to assess whether [<sup>11</sup>C]flumazenil is a P-glycoprotein substrate in humans and to what extent increased P-glycoprotein function in epilepsy may confound interpretation of clinical [<sup>11</sup>C]flumazenil studies used to assess gamma-aminobutyric acid A receptors.
The genetic polymorphism of ABCB1rs1045642 was found to be associated with normalized OXC concentration and therapeutic efficacy in patients with epilepsy (P<0.05).
By compared to the epilepsy model group, the P-gp expression was not markedly attenuated by the inhibition of NF-κB activity with PDTC treatment, nevertheless with a decrease of NF-κB expression in this intervention group.