Sinapic acid induces cytoplasmic stress granule formation, ER stress and apoptosis mediated anticancer activity in human endometrial cancer cell lines.

This study aimed to examine the impact of molecular mechanisms in endometrial cancer cell lines (Ishikawa and HEC-1-B) treated with sinapic acid (SA), which may have effect on regulation of genes in various processes including unfolded protein response and apoptosis. The impact of SA on cell viability was assessed through the XTT assay. Expressions of genes in apoptosis and endoplasmic reticulum (ER) stress pathways were evaluated using qPCR and western blot analyses. Effects of SA on colony formation and ER structure were determined using colony assay and transmission electron microscopy (TEM) visualization. The results showed a significant upregulated expression of CASP7, CASP8, CASP9, P53, ATF6, Eif2a, HSP47, IRE1 and PERK genes in Ishikawa cells. In HEC-1-B cells, expression of CASP3, CASP8, CYCS, FAS, P53, ATF6, CALR, CHOP, Eif2a, GRP78, HSP47, IRE1 and XBP1 genes were significantly increased, however FADD levels were decreased. Western blot analysis illustrated that comparing to the control CASP9 and CASP8 protein levels were increased in Ishikawa and in HEC-1-B cell lines, respectively. SA significantly suppressed colony formation capacities in both cell lines. TEM analyses also demonstrated that SA induced cytoplasmic stress granule formation in both cell lines. Therefore, this study suggested that SA can be a potential anticancer therapeutic agent for endometrial cancer.