Parthenolide and costunolide decrease detyrosinated tubulin in human breast carcinoma cells. (A) Bt‒549 (N = 3) and MDA‒MB‒157 (N = 6) cells treated for six hours with DMSO (Veh; 0.1%), parthenolide (Parth; 5 μM, 10 μM, 25 μM), costunolide (Cost; 5 μM, 10 μM, 25 μM), resveratrol (ResV; 50 μg/ml), colchicine (Col; 50 μM), and Taxol (Tax; 0.5 μg/ml). Parthenolide (10 μM, 25 μM), costunolide (10 μM, 25 μM), and colchicine (50 μM) significantly reduced detyrosinated tubulin (Detyr) levels compared to vehicle (*P <0.05; ** P <0.001, t‒test). Resveratrol, a non‒sesquiterpene lactone NF‒κB inhibitor, did not significantly affect detyrosinated tubulin (P >0.5, t‒test). Taxol significantly increased detyrosinated tubulin (‡Bt‒549 Tax value is × 2.5; MDA‒MB‒157 Tax value is × 10). None of the compounds induced apoptosis in these cells, as gauged by PARP cleavage. Columns, mean densitometry for N = 3 (Bt‒549) or N = 6 (MDA‒MB‒157) experiments; bars, SD. (B) Comparison of the compounds used show parthenolide and costunolide, two sesquiterpene lactones, are structurally similar while the other compounds are structurally dissimilar. DMSO, dimethyl sulfoxide; NF-κB, nuclear factor-kappaB; PARP, poly(ADP-ribose) polymerase.