Accumulation of poly (adenosine diphosphate-ribose) by sustained supply of calcium inducing mitochondrial stress in pancreatic cancer cells

Figure 4 Confirmation of poly-adenosine diphosphate ribose accumulation in pancreatic cancer cells (AsPC-1 and CFPAC-1) by calcium-mediated proteasomal activity. A: Quantitative analysis of poly adenosine diphosphate-ribose glycohydrolase (PARG) levels in AsPC-1; B: Quantitative analysis of PARG levels in CFPAC-1; C: Quantitative analysis of ADP-ribosyl hydrolase 3 (ARH3) levels in AsPC-1; D: Quantitative analysis of ARH3 levels in CFPAC-1; E: Quantitative analysis of PAR levels in AsPC-1; F: Quantitative analysis of PAR levels in CFPAC-1; G: Quantitative analysis of apoptosis-inducing factor (AIF) levels in AsPC-1; H: Quantitative analysis of AIF levels in CFPAC-1. Calpeptin was used for proteasome inhibition. The cells were treated with 2.5 mM lactate calcium salt for 72 h. Results represent the mean ± SD. ^aP < 0.001 vs untreated. CaLac: Lactate calcium salt; PARG: Poly adenosine diphosphate-ribose glycohydrolase; ARH3: Adenosine diphosphate-ribosyl hydrolase 3; AIF: Apoptosis-inducing factor.