Background: Okanin, a flavonoid compound derived fromBidens pilosaL., has garnered attention for its anti-inflammatory properties. AlthoughBidens pilosais commonly used in healthcare products and functional foods, the anticancer potential of okanin, particularly in oral cancer, remains underexplored. This study aims to investigate the effects of okanin on oral cancer cell lines and its potential as a therapeutic agent. Methods: The study involved assessing the cytotoxic effects of okanin on oral cancer cell lines SAS, SCC25, HSC3, and OEC-M1. The IC50 values were determined using methylene blue assays, and the clonogenic capacity was evaluated through colony formation assays. Flow cytometry was used to analyze cell cycle progression and apoptosis. Caspase-3/7 activity assays and annexin V/7-AAD staining confirmed the induction of apoptosis and pyroptosis. In vivo efficacy was assessed using a SAS xenograft model, and immunohistochemical analysis of xenograft tissue was performed to examine pyroptosis-related markers. Results: Okanin exhibited potent cytotoxic effects with IC50 values of 12.0 ± 0.8, 58.9 ± 18.7, 18.1 ± 5.3, and 43.2 ± 6.2 μM in SAS, SCC25, HSC3, and OEC-M1 cells, respectively. It caused dose- and time-dependent reductions in cell viability and significantly impaired clonogenic capacity. Flow cytometry revealed G2/M cell cycle arrest and increased sub-G1 population, indicating cell cycle disruption and death. Okanin induced both apoptosis and pyroptosis, as confirmed by caspase-3/7 activity and annexin V/7-AAD staining. In vivo, okanin reduced tumor growth and involved pyroptosis-related markers such as CASP1, GSDMC, GSDMD, and GSDME. Conclusions: Okanin demonstrates significant anticancer potential, particularly in oral cancer, by inducing both apoptosis and pyroptosis. Its efficacy in reducing tumor growth in vivo further supports its potential as a novel therapeutic option. Further mechanistic studies are needed to elucidate the pathways involved in okanin-mediated cell death and to explore its clinical applications.
背景：奥卡宁是一种从鬼针草中提取的黄酮类化合物，因其抗炎特性而受到关注。尽管鬼针草常用于保健品和功能性食品，但奥卡宁的抗癌潜力，特别是在口腔癌中的作用，仍未得到充分研究。本研究旨在探讨奥卡宁对口腔癌细胞系的影响及其作为治疗药物的潜力。方法：本研究评估了奥卡宁对口腔癌细胞系SAS、SCC25、HSC3和OEC-M1的细胞毒性作用。通过亚甲基蓝法测定IC50值，并通过集落形成实验评估克隆形成能力。流式细胞术用于分析细胞周期进程和细胞凋亡。Caspase-3/7活性测定和膜联蛋白V/7-AAD染色证实了细胞凋亡和细胞焦亡的诱导。使用SAS异种移植模型评估体内疗效，并对异种移植组织进行免疫组化分析以检测细胞焦亡相关标志物。结果：奥卡宁在SAS、SCC25、HSC3和OEC-M1细胞中表现出显著的细胞毒性作用，IC50值分别为12.0 ± 0.8、58.9 ± 18.7、18.1 ± 5.3和43.2 ± 6.2 μM。它引起细胞活力的剂量和时间依赖性降低，并显著削弱克隆形成能力。流式细胞术显示G2/M期细胞周期阻滞和亚G1期细胞比例增加，表明细胞周期紊乱和细胞死亡。Caspase-3/7活性和膜联蛋白V/7-AAD染色证实奥卡宁同时诱导细胞凋亡和细胞焦亡。在体内，奥卡宁抑制肿瘤生长，并涉及细胞焦亡相关标志物如CASP1、GSDMC、GSDMD和GSDME。结论：奥卡宁通过诱导细胞凋亡和细胞焦亡，显示出显著的抗癌潜力，特别是在口腔癌中。其在体内抑制肿瘤生长的效果进一步支持其作为一种新型治疗选择的潜力。需要进一步的机制研究来阐明奥卡宁介导细胞死亡的途径，并探索其临床应用。
Okanin Inhibits Cell Growth and Induces Apoptosis and Pyroptosis in Oral Cancer
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