In Vitro |
MT 63-78 (0-50 μM; 4 days; LNCaP and PC3 cells) treatment shows a dose-dependent decrease in cell number, and concomitant to the activation of AMPK signaling[1]. MT 63-78 (25 μM; 24 hours; LNCaP and CRPC cells) treatment induces a significant enrichement in the G2/M population[1]. MT 63-78 (0-50 μM; 24 hours; LNCaP, PC3, C4-4, C4-2B, CL1and 22RV1cells) treatment induces reduction of anti-apoptotic Mcl-1 in concert with accumulation of the pro-apoptotic BH3-only protein Puma[1]. MT 63-78 (0-50 μM; 30 minutes; LNCaP and PC3 cells) treatment shows a dose-dependent phosphorylation of the two major AMPK targets Acetyl-CoA Carboxylase (ACC) on Ser79 and of Raptor on Ser792. And also increases Thr172 phosphorylation on the AMPK α subunit[1]. Cell Viability Assay[1] Cell Line: LNCaP and PC3 cells Concentration: 0 μM, 1 μM, 5 μM, 10 μM, 25 μM, 50 μM Incubation Time: 4 days Result: A dose-dependent decrease in cell number, concomitant to the activation of AMPK signaling was observed. Cell Cycle Analysis[1] Cell Line: LNCaP and CRPC cells Concentration: 25 μM Incubation Time: 24 hours Result: Induced a significant enrichement in the G2/M population in both androgen sensitive and CRPC cell models. Apoptosis Analysis[1] Cell Line: LNCaP, PC3, C4-4, C4-2B, CL1and 22RV1cells Concentration: 0 μM, 10 μM, 25 μM, 50 μM Incubation Time: 24 hours Result: Induced reduction of anti-apoptotic Mcl-1 in concert with accumulation of the pro-apoptotic BH3-only protein Puma in all PCa cells. Western Blot Analysis[1] Cell Line: LNCaP and PC3 cells Concentration: 0 μM, 0.25 μM, 0.5 μM, 1 μM, 5 μM, 25 μM, 50 μM Incubation Time: 30 minutes Result: Observed a dose-dependent phosphorylation of the two major AMPK targets Acetyl-CoA Carboxylase (ACC) on Ser79 and of Raptor on Ser792. A corresponding increase in Thr172 phosphorylation on the AMPK α subunit was also observed.
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