{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T17:16:50Z","timestamp":1772212610882,"version":"3.50.1"},"reference-count":50,"publisher":"MDPI AG","issue":"3","license":[{"start":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T00:00:00Z","timestamp":1772150400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Basic Science Research Program through the National Research Foundation (NRF) of Korea, funded by the Ministry of Education","award":["NRF2022R1F1A1069376"],"award-info":[{"award-number":["NRF2022R1F1A1069376"]}]},{"name":"Soonchunhyang University Research Fund of Soonchunhyang University","award":["2026-0003"],"award-info":[{"award-number":["2026-0003"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["CIMB"],"abstract":"<jats:p>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.<\/jats:p>","DOI":"10.3390\/cimb48030258","type":"journal-article","created":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T15:52:38Z","timestamp":1772207558000},"page":"258","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Genistein\u2013Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells"],"prefix":"10.3390","volume":"48","author":[{"given":"Moon-Kyun","family":"Cho","sequence":"first","affiliation":[{"name":"Division of Molecular Cancer Research, Soonchunhyang Medical Research Institute, Soonchunhyang University, Cheonan 31511, Republic of Korea"},{"name":"Department of Dermatology, Soonchunhyang University Hospital, Seoul 04401, Republic of Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yeji","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheonan 31511, Republic of Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sang-Han","family":"Lee","sequence":"additional","affiliation":[{"name":"Division of Molecular Cancer Research, Soonchunhyang Medical Research Institute, Soonchunhyang University, Cheonan 31511, Republic of Korea"},{"name":"Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheonan 31511, Republic of Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hae-Seon","family":"Nam","sequence":"additional","affiliation":[{"name":"Division of Molecular Cancer Research, Soonchunhyang Medical Research Institute, Soonchunhyang University, Cheonan 31511, Republic of Korea"},{"name":"Department of Tropical Medicine, College of Medicine, Soonchunhyang University, Cheonan 31511, Republic of Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6364-1284","authenticated-orcid":false,"given":"Yoon-Jin","family":"Lee","sequence":"additional","affiliation":[{"name":"Division of Molecular Cancer Research, Soonchunhyang Medical Research Institute, Soonchunhyang University, Cheonan 31511, Republic of Korea"},{"name":"Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheonan 31511, Republic of Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2026,2,27]]},"reference":[{"key":"ref_1","first-page":"17","article-title":"Cancer statistics, 2023","volume":"73","author":"Siegel","year":"2023","journal-title":"CA Cancer J. 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