İbrahim Uğur ÇALIŞ, Esin Sakallı ÇETİN
European Journal of Therapeutics - 2026;32(4):420-427
Objective: Estrogen receptor-positive (ER+) breast and endometrial cancers are driven by estrogen-responsive transcriptional networks involving estrogen receptor 1 (ESR1) and regulatory long non-coding RNAs. We investigated the dose-dependent effects of silibinin on cell behavior and ESR1/long intergenic non-coding RNA 00511 (LINC00511) expression in ER+ cancer cell models. Methods: MCF-7 breast cancer cells and Ishikawa endometrial cancer cells were exposed to graded concentrations of silibinin. Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, wound closure by scratch (wound-healing) assay, and apoptosis by Annexin V/propidium iodide (PI) staining. ESR1 and LINC00511 transcript levels were quantified using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Half-maximal inhibitory concentration (IC50) values were calculated from viability data. Results: Lower silibinin concentrations increased cell viability and wound closure and were accompanied by higher ESR1 and LINC00511 expression. In contrast, higher concentrations suppressed ESR1 and LINC00511, reduced wound closure, and increased apoptosis. The IC50 values were 193 µM for MCF-7 cells and 263 µM for Ishikawa cells. Conclusion: Silibinin elicited a biphasic, dose-dependent response in ER-positive breast and endometrial cancer cells. These findings suggest that the biological effects of silibinin in ER-positive tumor models should be interpreted in a dose-dependent context.
