Yang Xiaonan, Ding Zhimin, Hua Hongting, Gan Ruijia, Meng Dongdong, Zang Yan, Xiao Han, Wang Dong, Jiang Wanjin, Si Dongyu, Wei Xiang, Zhang Mei, Zhang Huabing, Gao Chaobing
Department of Otorhinolaryngology Head and Neck Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China.
Department of Otorhinolaryngology Head and Neck Surgery, Fuyang Women and Children's Hospital, Fuyang, 236000, China.
J Cancer. 2025 Mar 31;16(7):2339-2352. doi: 10.7150/jca.92956. eCollection 2025.
The present study aimed to explore the underlying antitumor effects of bavachin on laryngopharyngeal cancer and . Tu212 and FaDu cells were cultured in the incubator. Cells were treated with 0.1% DMSO (control group) and different concentrations of bavachin (experimental groups) for exploring the results of proliferation and apoptosis. We revealed the underlying mechanism of bavachin on laryngopharyngeal cancer through western blotting, qRT-PCR assay and immunofluorescence staining. Bavachin could suppress the proliferation and migration of laryngopharyngeal cancer cells and . Mechanistically, the results suggested that bavachin could downregulate the phosphorylation level of the signal transducer and activator of the transcription 3 (STAT3) and upregulate those of the mitogen-activated protein kinase (MAPK). Furthermore, bavachin also increased the expression level of Bax and suppressed those of Bcl-2, CDK4/6, and CyclinD1 in the laryngopharyngeal cancer cells. Additionally, the study also identified that bavachin promoted ferroptosis by decreasing the expression level of glutathione peroxidase 4 (GPX4) and increasing those of intracellular reactive oxygen species (ROS) and glutathione (GSH). Taken together, these results demonstrated that bavachin could suppress the growth and migration of laryngopharyngeal cancer cells and induce apoptosis and cell cycle arrest of the laryngopharyngeal cancer cells by regulating the MAPK/STAT3 signaling pathway. This study demonstrated that bavachin exhibited a clinical therapeutic potential for laryngopharyngeal cancer.
本研究旨在探讨补骨脂素对喉咽癌的潜在抗肿瘤作用。将Tu212和FaDu细胞在培养箱中培养。用0.1%二甲基亚砜（对照组）和不同浓度的补骨脂素（实验组）处理细胞，以探究增殖和凋亡结果。我们通过蛋白质免疫印迹法、qRT-PCR检测和免疫荧光染色揭示了补骨脂素对喉咽癌的潜在作用机制。补骨脂素可抑制喉咽癌细胞的增殖和迁移。从机制上讲，结果表明补骨脂素可下调信号转导和转录激活因子3（STAT3）的磷酸化水平，并上调丝裂原活化蛋白激酶（MAPK）的磷酸化水平。此外，补骨脂素还可增加喉咽癌细胞中Bax的表达水平，并抑制Bcl-2、CDK4/6和细胞周期蛋白D1的表达。此外，该研究还发现补骨脂素通过降低谷胱甘肽过氧化物酶4（GPX4）的表达水平，增加细胞内活性氧（ROS）和谷胱甘肽（GSH）的水平来促进铁死亡。综上所述，这些结果表明补骨脂素可通过调节MAPK/STAT3信号通路抑制喉咽癌细胞的生长和迁移，并诱导喉咽癌细胞凋亡和细胞周期阻滞。本研究表明补骨脂素对喉咽癌具有临床治疗潜力。
