DTHIB is a direct and selective inhibitor of heat shock factor 1 (HSF1) with a Kd of 160 nM for binding to the HSF1 DNA binding domain (DBD). It inhibits the HSF1 cancer gene signature (HSF1 CaSig) and selectively promotes the degradation of nuclear HSF1, exhibiting potent anticancer activities that can be utilized in prostate cancer research [1].
体内研究
DTHIB (5 mg/kg; intraperitoneal injection; daily; for 3 weeks) potently inhibits tumor progression in a C4-2 xenograft mouse model [1].
体外研究
C4-2 cells with DTHIB (5 μM; 48 hours) induces cell cycle arrest, leading to accumulation in the G1 phase, and stimulates entry into senescence [1].
DTHIB (0.5-5 μM; 48 hours), in C4-2 prostate cancer cells, reduces the steady-state protein levels of molecular chaperones P23, HSP27, HSP70, and HSP90, all of which are bona fide HSF1 targets [1].
DTHIB demonstrates dose-dependent reduction in clonal expansion for both C4-2 and PC-3 PCa cells, with EC50 values of 1.2 μM and 3.0 μM, respectively [1].
DTHIB (0.5-10 μM) dose-dependently attenuates the robust acute heat shock induction of HSP70 and HSP25 molecular chaperones in mouse embryonic fibroblasts (MEFs). This attenuation occurs by reducing the steady-state transcript abundance of multiple molecular chaperones [1].
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