Isoalantolactone exerts anticancer effects on human HEC-1-B endometrial cancer cells via induction of ROS mediated apoptosis and inhibition of MEK/ERK signalling pathway
Isoalantolactone has been shown to inhibit the growth of different cancer cells. The objective of the present study was to evaluate the effects of isoalantolactone on the proliferation of endometrial cancer HEC-1-B cells. Results showed that isoalantolactone suppressed the proliferation of HEC-1-B cells in a concentration-dependent manner and exhibited an IC50 of 10 µM. The cytotoxic effects of isoalantolactone were relatively lower against the normal THESC cells. Mechanistic studies revealed apoptosis to be responsible for the isoalantolactone mediated antiproliferative effects. Annexin V/PI assay showed that the percentage of the apoptotic HEC-1B cells increased from 3.74% in untreated cells to 28.9% at 20 µM isoalantolactone. The expression of Bax was significantly increased and that of Bcl-2 was decreased in isoalantolactone treated HEC-1B cells. Analysis of ROS levels revealed that the ROS levels of HEC-1B cells increased with the increase in concentration of isoalantolactone. The ROS levels increased to 210% of the control at 20 µM isoalantolactone. The wound healing and the transwell assays showed that migration and invasion of the HEC-1B cells was significantly decreased upon isoalantolactone treatment. Finally, the effects of isoalantolactone were also evaluated on the MEK/ERK signalling pathway. It was found that isoalantolactone could concentration-dependently block the expression of p-MEK and p-ERK. Taken together, the results suggest that isoalantolactone could prove to be a lead molecule in the development of chemotherapy for endometrial cancer.
Copyright (c) 2022 Fang Hu, Ping Yang
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
Acta Biochimica Polonica is an open access quarterly and publishes four issues a year. All contents are distributed under the Creative Commons Attribution-ShareAlike 4.0 International (CC BY-SA 4.0) license. Everybody may use the content following terms: Attribution — You must give appropriate credit, provide a link to the license, and indicate if changes were made, ShareAlike — If you remix, transform, or build upon the material, you must distribute your contributions under the same license as the original. There are no additional restrictions — You may not apply legal terms or technological measures that legally restrict others from doing anything the license permits.
Copyright for all published papers © stays with the authors.
Copyright for the journal: © Polish Biochemical Society.