Boric Acid Shows ER Stress and Apoptosis Mediated Anticancer Activity in Human Pancreatic Cancer MIA PaCa-2 and PANC-1 Cells

Aim: Objective of this study was to investigate the endoplasmic reticulum (ER) stress and apoptosis mediated anticancer ef fect of boric acid in human pancreatic cancer MIA PaCa-2 and P ANC-1 cells. Materials and Methods: The effect of boric acid on the viability of pancreatic cancer cells and the IC50 value were calculated by XTT test and using CompuSyn version 1.0 software. Apoptotic, anti-apoptotic and ER stress-related gene levels were determined. The effect of boric acid on the colony formation capacity of these cells was evaluated with the colony formation assay.
Results: Boric acid inhibited cell viability in these cell lines as time and dose dependent. As a result of the XTT test, the IC50 doses of boric acid in MIA PaCa-2 and PANC-1 cells were found to be 15707.5 and 14248.8 μM, respectively. Boric acid significantly upregulated BAX, CASP3, CASP8, CYCS and FAS expression, which are the genes associated with apoptosis in both cell lines. CASP9 and FADD gene levels were significantly elevated only in PANC-1 cells. It was observed that boric acid statistically upregulated the expression of ATF4, HSP47 and XBP1 genes associated with ER stress in both cell lines. In addition, boric acid treatment significantly increased ATF6, CHOP and EIF2A expressions only in PANC-1 cells. Boric acid also caused an increase in GRP78 gene expression in MIA PaCa-2 cells. Colony formation test results illustrated that boric acid significantly suppressed co lony formation capacities in both cell lines.
Conclusion: Boric acid reduced cell viability and colony formation in both human pancreatic cancer cells and changed gene levels in apoptosis and ER stress pathways. Findings suggested that boric acid exhibits anticancer activity in human pancreatic cancer cells v ia ER stress and apoptosis.