Current oncology (Toronto, Ont.) · 2025
Cytotoxicity of Esculetin Compared with Vinblastine and Paclitaxel in PC-3 Prostate Cancer Cells.
СтатьяСравнительное исследованиеНазвание и аннотация: Перевод в очереди
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García-Pérez Ana I, Rubio Virginia, Herráez Angel, Puebla Lilian, Diez José C
Аннотация
BACKGROUND/OBJECTIVES: Metastatic prostate cancer is among the therapy-resistant human neoplasms. PC-3 is a commonly used experimental cell line that does not express androgen receptors. We compared the cytotoxicity of esculetin with that of vinblastine and paclitaxel on prostatic tumour PC-3 cells.
METHODS: Cells were treated with either esculetin (100 or 250 μM), vinblastine (50 μM) or paclitaxel (100 or 200 μM) for 19 to 72 h. Cells were assessed for metabolic viability, membrane integrity, DNA fragmentation and cell cycle analysis. Apoptosis was checked with annexin and propidium iodide.
RESULTS: Esculetin decreased the metabolic activity of PC-3 cells in a time- and concentration-dependent way. The metabolic activity of vinblastine- and paclitaxel-treated cells did not show time-dependence. Cells treated with 250 µM esculetin for 48 or 72 h showed apoptosis levels similar to those produced by 50 µM vinblastine at these incubation times or by 200 µM paclitaxel at 19 h. Vinblastine and paclitaxel produced cell cycle arrest in the G2/M phase after incubation for 19 h. In contrast, esculetin did not significantly affect the cell cycle.
CONCLUSIONS: A differential action of esculetin on PC-3 prostate cells may be inferred. This may be relevant for novel therapies against resistant prostate cancer.
METHODS: Cells were treated with either esculetin (100 or 250 μM), vinblastine (50 μM) or paclitaxel (100 or 200 μM) for 19 to 72 h. Cells were assessed for metabolic viability, membrane integrity, DNA fragmentation and cell cycle analysis. Apoptosis was checked with annexin and propidium iodide.
RESULTS: Esculetin decreased the metabolic activity of PC-3 cells in a time- and concentration-dependent way. The metabolic activity of vinblastine- and paclitaxel-treated cells did not show time-dependence. Cells treated with 250 µM esculetin for 48 or 72 h showed apoptosis levels similar to those produced by 50 µM vinblastine at these incubation times or by 200 µM paclitaxel at 19 h. Vinblastine and paclitaxel produced cell cycle arrest in the G2/M phase after incubation for 19 h. In contrast, esculetin did not significantly affect the cell cycle.
CONCLUSIONS: A differential action of esculetin on PC-3 prostate cells may be inferred. This may be relevant for novel therapies against resistant prostate cancer.