Chia Wei-Tso, Chen Kuei-Yuan, Yang Cheng-Yu, Hsieh Cheng-Chih, Tsao Chang-Huei, Lin Chih-Kung, Peng Bo, Ho Sien-Lin, Chen Yi-Ling, Chang Szu-Chien, Chen Yuan-Wu
Department of Orthopedics, National Taiwan University Hospital Hsin-Chu Branch, Hsinchu 302, Taiwan.
Department of Nursing, Yuan Pie University of Medical Technology, Hsinchu 302, Taiwan.
Cancers (Basel). 2024 Sep 19;16(18):3195. doi: 10.3390/cancers16183195.
Okanin, a flavonoid compound derived from L., has garnered attention for its anti-inflammatory properties. Although is 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.
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.
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.
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.
奥卡宁是一种从[植物名称]中提取的黄酮类化合物，因其抗炎特性而受到关注。尽管奥卡宁常用于保健品和功能性食品中，但其抗癌潜力，尤其是在口腔癌中的潜力，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剂的潜力。
该研究涉及评估奥卡宁对口腔癌细胞系SAS、SCC25、HSC3和OEC-M1的细胞毒性作用。使用亚甲蓝测定法确定IC50值，并通过集落形成试验评估克隆形成能力。采用流式细胞术分析细胞周期进程和凋亡情况。半胱天冬酶-3/7活性测定和膜联蛋白V/7-氨基放线菌素D染色证实了凋亡和焦亡的诱导。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织化学分析以检测焦亡相关标志物。
奥卡宁在SAS、SCC25、HSC3和OEC-M1细胞中分别表现出强大的细胞毒性作用，IC50值分别为12.0±0.8、58.9±18.7、18.1±5.3和43.2±6.2μM。它导致细胞活力呈剂量和时间依赖性降低，并显著损害克隆形成能力。流式细胞术显示G2/M期细胞周期阻滞和亚G1期细胞群体增加，表明细胞周期紊乱和死亡。半胱天冬酶-3/7活性和膜联蛋白V/7-氨基放线菌素D染色证实奥卡宁诱导了凋亡和焦亡。在体内，奥卡宁减少了肿瘤生长，并涉及焦亡相关标志物，如CASP1、GSDMC、GSDMD和GSDME。
奥卡宁通过诱导凋亡和焦亡显示出显著的抗癌潜力，尤其是在口腔癌中。其在体内减少肿瘤生长的疗效进一步支持了其作为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的细胞死亡所涉及的途径，并探索其临床应用。
