BACKGROUND : Autophagy can either be protective and confer survival to stressed cells, or it can contribute to cell
death. The antimitotic drug 2-ethyl-3-O-sulpamoyl-estra-1,3,5(10),15-tetraen-17-ol (ESE-15-ol) is an in silico-designed
17-β-estradiol analogue that induces both autophagy and apoptosis in cancer cells. The aim of the study was to
determine the role of autophagy in ESE-15-ol-exposed human adenocarcinoma breast cancer cells; knowledge that
will contribute to future clinical applications of this novel antimitotic compound. By inhibiting autophagy and determining
the cytotoxic effects of ESE-15-ol-exposure, deductions could be made as to whether the process may confer
resistance to the drug, or alternatively, contribute to the cell death process.
METHODS AND RESULTS : Spectophometrical analysis via crystal violet staining was used to perform cytotoxicity studies.
Morphology studies were done using microscopic techniques namely polarization-optical transmitted light differential
interference light microscopy, fluorescent microscopy using monodansylcadaverine staining and transmission
electron microscopy. Flow cytometry was used to quantify the autophagy inhibition and assess cell viability. Results
obtained indicated that 3-methyladenine inhibited autophagy and increased cell survival in both MCF-7 and MDAMB-
231 cell lines.
CONCLUSION : This in vitro study inferred that autophagy inhibition with 3-methyladenine does not confer increased
effectiveness of ESE-15-ol in inducing cell death. Thus it may be concluded that the autophagic process induced by
ESE-15-ol exposure in MCF-7 and MDA-MB-231 cells plays a more significant role in cell death than conferring survival.