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. 2016 Jul 22;7(35):56767–56780. doi: 10.18632/oncotarget.10790

Figure 5. The silencing or C-terminal mutation of HDAC3 activates the expression of p21 and BAX by inducing oligomerization of p53.

Figure 5

A. HDAC3 silencing increased expression of BAX and p21 in delphinidin–treated LNCaP cells. HDAC3 siRNA was transfected into LNCaP cells with delphinidin. B. Co-treatment with delphinidin and HDAC3 siRNA reduced cell viability, which was measured using the MTT assay. All data are expressed as the mean ± SD for triplicate measurements. Statistical significance was determined using Student's t-test; *P < 0.01 versus HDAC3 siRNA-treated LNCaP cells. C. HDAC3 silencing enhanced p53 oligomerization. D, E. HDAC3wt and HDAC3D391A inhibited cell viability during delphinidin-mediated apoptosis. D. Delphinidin–treated LNCaP cell extracts were analyzed by western blot analysis using the indicated antibodies. E. The cell viability was measured using the MTT assay. All data are expressed as the mean ± SD for triplicates. Statistical significance was determined using Student's t-test; *P < 0.01 versus delphinidin-treated LNCaP cells. F. HDAC3 over-expression inhibited p53 oligomerization.