Genistein-Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells.
1/5 보강
Prostate cancer progression involves metabolic reprogramming that supports sustained proliferation and survival, highlighting metabolic pathways as potential targets for intervention.
APA
Cho MK, Lee Y, et al. (2026). Genistein-Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells.. Current issues in molecular biology, 48(3). https://doi.org/10.3390/cimb48030258
MLA
Cho MK, et al.. "Genistein-Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells.." Current issues in molecular biology, vol. 48, no. 3, 2026.
PMID
41899410 ↗
Abstract 한글 요약
Prostate cancer progression involves metabolic reprogramming that supports sustained proliferation and survival, highlighting metabolic pathways as potential targets for intervention. While genistein (GEN) and butein (BTN) are naturally occurring polyphenolic compounds with reported anticancer activities, their combined effects on prostate cancer cell metabolism and apoptotic signaling remain unclear. Here, we investigated the effects of GEN and BTN, administered individually and in combination, on human PC-3 prostate cancer cells, with normal human prostate epithelial cells (HPrEC) used for comparison. Cell viability was assessed using MTT and trypan blue exclusion assays. Glycolytic metabolism was evaluated by measuring glucose consumption, lactate production, hexokinase and pyruvate dehydrogenase activity, and intracellular ATP levels, while apoptotic and survival signaling pathways were analyzed by means of Annexin V staining and Western blotting. GEN/BTN co-treatment selectively reduced PC-3 cell viability, producing greater inhibitory effects than either compound alone. This enhanced response was accompanied by suppression of glycolytic metabolism, ATP depletion, attenuation of AKT and ERK phosphorylation, and activation of apoptotic signaling, as evidenced by increased cleavage of caspase-3 and PARP. Collectively, these findings indicate that GEN/BTN co-treatment cooperatively disrupts glycolytic metabolism while activating apoptotic signaling in prostate cancer cells.
🏷️ 키워드 / MeSH 📖 같은 키워드 OA만
🏷️ 같은 키워드 · 무료전문 — 이 논문 MeSH/keyword 기반
- Comprehensive analysis of androgen receptor splice variant target gene expression in prostate cancer.
- Constitutive NF-kB Activation Is Amplified by VSV in Aggressive PC3 Prostate Cancer Cells That Resist Viral Oncolysis.
- Halogen substituted 4-thio-2'-deoxyuridines as photosensitizers for the photodynamic therapy of prostate cancer. An in vitro study.
- Inhibition of c-FLIP alongside TRAIL treatment suppresses prostate cancer stem cell activity.
- Eco-Friendly Combat against Prostate Cancer: Green Chemistry Approach Using Biosynthesized Nanoparticles Functionalized with Propolis for Enhanced Anticancer Activity.
- Tumor control probability analysis in carbon-ion radiotherapy for prostate cancer considering the oxygen effect.