Autophagy Induction by α-Santalol in Human Prostate Cancer Cells

Background/aim Previous studies have shown that the sandalwood oil constituent α-santalol inhibits growth of cultured human prostate cancer cells in vitro and PC-3 xenografts. Along with from our laboratory, it is well established targets phosphatidylinositol-4,5-bisphosphate 3-kinase-AKT serine/ threonine kinase 1 (AKT) pathway to induce apoptosis but its growth-suppressive effects not been fully elucidated. The current study was undertaken investigate role autophagy α-santalol-induced cell death. Materials methods Cell lines LNCaP were maintained an atmosphere 95% air 5% CO2 at 37°C. Trypan blue dye exclusion assay employed assess with/without 3-methyl adenine on viability cells. Acidic vesicular organelles induced by treatment detected staining acridine orange. Immunofluorescence immunoblotting performed analyze expression proteins involved AKT-mammalian target rapamycin (mTOR) pathway. Results upon resulted characteristic features analogous autophagic response, including formation acidic organelles, recruitment cleavage microtubule-associated protein light chain 3 (LC3) autophagosomes. Alpha-santalol further suppressed phosphorylation activated AKT mTOR, which are critical regulators response. In addition, pre-treatment specific inhibitor (3-methyladenine) co-treatment attenuated LC3-II phospho-AKT, significantly reduced viability. Conclusion present indicates induces targeting AKT-mTOR cells, may serve as a protective mechanism.