Escin induces apoptosis in ovarian cancer cell line by triggering S-phase cell cycle arrest and p38 MAPK/ERK pathway inhibition

Background: Ovarian cancer (OC), is a common malignant tumors in the female reproductive system with the increased mortality rate. The occurrence of OC is elevating rapidly in recent decades. Escin is a triterpene saponin reported to possess the significant biological activities. Objective: The current investigation focused to address the in vitro anticancer actions of escin against the OC A2780 cells through the inhibition of p38 MAPK/ERK pathway. Methodology: The in vitro antioxidant potential of escin was examined using different free radicals scavenging assays like reducing power, DPPH, and superoxide radicals. Escin treated Vero and A2780 cell's viability was investigated by MTT assay. The lipid peroxidation, antioxidants SOD and GSH was quantified in the escin treated A2780 cells were by standard methods. The effect of escin on the ROS accumulation, MMP, and apoptotic cell death in A2780 cells was scrutinized by respective fluorescence staining assays. The cell cycle transition was studied by flow cytometry and the expressions of p38 MAPK/ERK molecules were investigated using RT-PCR analysis. Results: Escin possessed the appreciable reducing power and scavenged the DPPH and superoxide radicals, which proves the antioxidant capacity of escin. The viability of A2780 cells was remarkably suppressed by the escin and it did not possessed toxicity to the normal Vero cells. Escin improved the lipid peroxidation and suppressed the SOD and GSH levels in the A2780 cells. The status of MMP was substantially decreased and the ROS and apoptotic cells were drastically elevated in the escin administered A2780 cells. Escin treatment notably suppressed the p38 MAPK/ERK signaling axis in the A2780 cells. Conclusion: The findings of this investigation have revealed that the escin has demonstrated the potent in vitro anticancer actions against the OC A2780 cells. (c) 2021 Published by Elsevier B.V. on behalf of King Saud University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).