KO-HSIU LUPEI-NI CHEN2026-10-162026-10-162014-05-19Pure ID: 15100286Pure UUID: 86b3bff8-91f7-4f3c-ac51-b27fec10b35f10.1080/01635581.2014.894100https://www.scopus.com/pages/publications/84899982866https://scholars.csmu.edu.tw/handle/123456789/32580Flavanones demonstrate a propensity to antiproliferation and induce apoptosis of malignant cells. Among the 4 flavanones under study, 2′-hydroxyflavanone exhibited the greatest potency to reduce the cell viability of 143 B cells in 4 osteosarcoma cells. Flow cytometry analysis showed that 2′-hydroxyflavanone increased the hypodiploid cells in the sub-G1 phase but resulted in the reduced DNA content in the G0/G1 phase in 143 B cells. The 2′-hydroxyflavanone-induced apoptosis in 143 B cells was confirmed by 4′-6-diamidino-2-phenylindole staining and mitochondrial membrane potential (Δψm) assay. Increasing expressions of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and death receptor 5 (DR5) were found in 2′-hydroxyflavanone-treated cells. Moreover, 2′-hydroxyflavanone increased the expressions of B-cell lymphoma-extra small, cytochrome c, and cleavage poly (ADP-ribose) polymerase but downregulated B-cell lymphoma/leukemia-2expressions in 143 B cells. Furthermore, in vivo experiments showed that 2′-hydroxyflavanone inhibited the tumor growth of 143 B cells. 2′-hydroxyflavanone induced the apoptosis of 143 B cells via the extrinsic TRAIL- and intrinsic mitochondrial-dependent pathways, indicating its potential for inducing cancer apoptosis in osteosarcoma.11enjournal article