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Researchers' findings from University of Cambridge advance research.
Study 1: Breast cancer resistance protein (BCRP) and p-glycoprotein could be modulated by certain prescribed corticosteroids.
"Efflux transporters, p-glycoprotein and BCRP, located at barrier sites such as the blood-brain barrier may affect distribution of steroids used for treating chronic inflammatory conditions and thus the extent to which they may perturb the hypothalamic-pituitary-adrenal axis. In the present study, 6 different glucocorticoids were investigated for their possible interactions with these efflux transporters," investigators in England reported.
"Beclomethasone dipropionate, mometasone furoate and ciclesonide active principle but not fluticasone propionate or triamcinolone, (all at .1 to 10 mcM) caused inhibition of efflux, resulting in increased accumulation of mitoxantrone in BCRP-expressing MCF7/MR breast cancer cells and of calcein in p-glycoprotein-expressing SW620/R colon carcinoma cell. At 5 mcM the same 3 increased sensitivity of p-glycoprotein-expressing SW620/R to doxorubicin and stimulated ATPase activity associated with BCRP expressed in bacterial membrane vesicles. Budesonide also stimulated ATPase activity," explained H.C. Cooray and colleagues, University of Cambridge.
The researchers concluded, "These data demonstrate the capacity of some clinically used glucocorticoids to interact with efflux transporters."