mibolerone and lambertianic-acid

Lambertianic acid (LA) is known to have anti-allergic and antibacterial effects. However, the anticancer activities and mechanism of action of LA have not been investigated. Therefore, the anticancer effects and mechanism of LA are investigated in this study. LA decreased not only AR protein levels, but also cellular and secretory levels of PSA. Furthermore, LA inhibited nuclear translocation of the AR induced by mibolerone. LA suppressed cell proliferation by inducing G₁ arrest, downregulating CDK4/6 and cyclin D1 and activating p53 and its downstream molecules, p21 and p27. LA induced apoptosis and the expression of related proteins, including cleaved caspase-9 and -3, c-PARP and BAX, and inhibited BCl-2. The role of AR in LA-induced apoptosis was assessed by using siRNA. Collectively, these findings suggest that LA exerts the anticancer effect by inhibiting AR and is a valuable therapeutic agent in prostate cancer treatment.

Topics: Antineoplastic Agents; Apoptosis; bcl-2-Associated X Protein; Carboxylic Acids; Caspase 3; Caspase 9; Cell Cycle Proteins; Cell Line, Tumor; Cell Proliferation; Cyclin D1; Cyclin-Dependent Kinase 4; Cyclin-Dependent Kinase 6; Down-Regulation; G1 Phase Cell Cycle Checkpoints; Humans; Nandrolone; Naphthalenes; Prostate-Specific Antigen; Proto-Oncogene Proteins c-bcl-2; Receptors, Androgen; RNA Interference; RNA, Small Interfering; Tumor Suppressor Protein p53