Journal: Current Issues in Molecular Biology

Article Title: Genistein–Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells

doi: 10.3390/cimb48030258

Figure Lengend Snippet: Genistein and butein reduce cell viability in prostate cancer cells. ( A ) Chemical structures of GEN and BTN. ( B ) Viability of PC-3 prostate cancer cells and HPrEC following exposure to increasing concentrations of GEN or BTN for 24 or 48 h, evaluated using the MTT assay. ( C ) Cell viability measured by means of trypan blue exclusion under identical treatment conditions. Results are normalized to untreated controls, and IC 50 values were calculated from 48 h treatment data where indicated. Values represent the mean ± SD of at least three independent experiments; * p < 0.05 versus control. HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein; Conc.: concentration.

Article Snippet: Human prostate cancer PC-3 cells and normal human prostate epithelial cells (HPrEC) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: MTT Assay, Control, Concentration Assay

Journal: Current Issues in Molecular Biology

Article Title: Genistein–Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells

doi: 10.3390/cimb48030258

Figure Lengend Snippet: Combined genistein and butein treatment impairs glycolytic metabolism in PC-3 cells. HPrEC and PC-3 cells were treated with GEN, BTN, or GEN/BTN for 48 h. ( A , B ) Extracellular lactate production and glucose consumption were quantified and normalized to control levels. Enzymatic activities of hexokinase (HK) and pyruvate dehydrogenase (PDH) were assessed following treatment. GEN/BTN co-treatment produced a pronounced suppression of glycolytic activity in PC-3 cells, whereas metabolic parameters in HPrEC cells remained largely unchanged. Data are shown as the mean ± SD (n = 3). Statistical significance is indicated by asterisks (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001). HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein.

Article Snippet: Human prostate cancer PC-3 cells and normal human prostate epithelial cells (HPrEC) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Control, Produced, Activity Assay

Journal: Current Issues in Molecular Biology

Article Title: Genistein–Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells

doi: 10.3390/cimb48030258

Figure Lengend Snippet: Genistein–butein co-treatment decreases ATP levels and clonogenic survival in PC-3 cells. ( A ) Intracellular ATP content was determined after 48 h exposure to GEN, BTN, or GEN/BTN, and expressed relative to control cells (n = 3 independent experiments). ( B ) Crystal violet staining images illustrating treatment-dependent changes in cell survival. ( C ) Quantitative analysis of crystal violet staining measured at 590 nm. Each dot represents an individual replicate, and data are presented as mean ± SD (total n = 8 pooled from at least three independent experiments). Following GEN/BTN co-treatment in PC-3 cells, a significant reduction in ATP production and cell survival was observed, while normal HPrEC cells showed minimal changes. Results represent the mean ± SD from three independent experiments. Statistical significance is indicated by asterisks (* p < 0.05; ** p < 0.01; **** p < 0.0001). HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein.

Article Snippet: Human prostate cancer PC-3 cells and normal human prostate epithelial cells (HPrEC) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Control, Staining

Journal: Current Issues in Molecular Biology

Article Title: Genistein–Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells

doi: 10.3390/cimb48030258

Figure Lengend Snippet: Genistein–butein co-treatment promotes apoptosis and suppresses AKT/ERK signaling in PC-3 cells. ( A ) Apoptotic cell populations were evaluated using Annexin V and viability staining after 48 h treatment. Representative dot plots are shown for HPrEC and PC-3 cells. ( B ) Expression levels of hexokinase II and PDH were analyzed by means of Western blotting, with β-actin serving as a loading control. Corresponding densitometric analyses are presented. ( C ) Phosphorylation status of AKT and ERK, along with levels of cleaved caspase-3 and cleaved PARP, was examined by Western blot analysis. GEN/BTN co-treatment selectively inhibited survival signaling and enhanced apoptotic marker cleavage in PC-3 cells. Data are presented as the mean ± SD. Statistical significance is indicated. Statistical significance is indicated by asterisks (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001). HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein; PDH: pyruvate dehydrogenase.

Article Snippet: Human prostate cancer PC-3 cells and normal human prostate epithelial cells (HPrEC) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Staining, Expressing, Western Blot, Control, Phospho-proteomics, Marker