Fig. 7
Sinularin induced prostate cancer cell apoptosis through autophagic degradation of survivin protein. (A) After apoptosis was inhibited by Z-VAD-FMK, the LC3 I/II, and p62 protein levels were determined via western blot analysis in Sinularin-treated LNCaP and PC-3 cells. (B) Western blot analysis of cleaved PARP and cleaved caspase 3 in Sinularin-treated LNCaP and PC-3 cells following the inhibition of autophagy by chloroquine (CHQ). (C) After autophagy was inhibited by chloroquine (CHQ), cell apoptosis was measured via flow cytometry (FCM) analysis in Sinularin-treated LNCaP and PC-3 cells. (D) Western blot analysis of survivin protein levels in Sinularin-treated LNCaP and PC-3 cells. (E) After autophagy was inhibited by chloroquine (CHQ), survivin protein level in Sinularin-treated LNCaP and PC-3 cells was determined by western blot analysis. (F) Cell apoptosis was measured by flow cytometry (FCM) analysis in Sinularin-treated LNCaP and PC-3 cells following the upregulation of survivin. (G) Western blot analysis of cleaved PARP and cleaved caspase 3 in Sinularin-treated LNCaP and PC-3 cells following the upregulation of survivin.
