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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: ZMAT1 acts as a tumor suppressor in pancreatic ductal adenocarcinoma by inducing SIRT3/p53 signaling pathway

Fig. 2

ZMAT1 inhibits proliferation and migration of Pancreatic Ductal Adenocarcinoma (PDAC) cells. A-B Real-time quantitative polymerase chain reaction (RT-qPCR) (A) and western blot (B) showed ZMAT1 was highly expressed in BXPC-3 and Capan-2 cells, while relatively low-expressed in SW1990 cells among PDAC cell lines. C RT-qPCR and western blot were used to detect the over-expression of ZMAT1 in SW1990 cells. D CCK-8 assays showed that ZMAT1 over-expression reduced the proliferation in SW1990 cells. E RT-qPCR and western blot were used to detect the down-regulation of ZMAT1 in BXPC-3 cells transfected with ZMAT1-siRNA. F CCK-8 assays showed that ZMAT1 down-regulation promoted the proliferation in BXPC-3 cells. G RT-qPCR and western blot were used to detect the down-regulation of ZMAT1 in Capan-2 cells transfected with ZMAT1-siRNA. H CCK-8 assays showed that ZMAT1 down-regulation promoted the proliferation in Capan-2 cells. I-K Colony formation assays showed that ZMAT1 over-expression reduced the proliferation in SW1990 cells (I), while ZMAT1 knockdown promoted the proliferation in BXPC-3 (J) and Capan-2 cells (K). L-N Transwell assays showed that ZMAT1 over-expression reduced the migration in SW1990 cells (L), while ZMAT1 knockdown promoted the migration in BXPC-3 (M) and Capan-2 cells (N). All * P-value < 0.05, ** P-value < 0.01, *** P-value < 0.001. Scale bars: 100 μm. P-values were assessed using two-tailed t-tests and ANOVA followed by Dunnett’s tests for multiple comparison in C-N. All figures represent mean ± SD from three independent experiments

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