Figure 8

Model of DGAT1 inhibition of lipid-MTOC axis in prostate cancer. This is a model of lipid-MTOC crosstalk in prostate cancer. At baseline, PCa cells are lipid-rich with MTOC amplification and a complex and dense MT network. At the site of the Golgi apparatus, GM130 and CLASP2-coated MTs are strongly expressed. PC-3 cells express high levels of DGAT1 and low levels of PEDF protein. After treatment with a DGAT1 inhibitor, the LD density is reduced as well as the number of MTOCs. The expression levels of proteins regulating ncMTOCs (GM130 and CLASP2) and MTOCs in general (γ-tubulin and ninein) were significantly decreased. Structural changes in the MT network post-treatment revealed fragmentation and loss of many linear MTs. Blockade of the lipid-MTOC axis via DGAT1 inhibitor resulted in suppression of prostate cancer growth and invasion both in vitro and in vivo.