Ye Ben, Ma Jianhua, Li Zhaoxia, Li Yang, Han Xiaopan
Department of Ear, Nose, and Throat (ENT), Shandong Provincial Hospital Affiliated to Shandong First Medical University, Ji'nan, China.
Department of Cardiology, Shandong Rongjun General Hospital, Ji'nan, China.
Front Oncol. 2022 Jul 14;12:939646. doi: 10.3389/fonc.2022.939646. eCollection 2022.
Laryngeal cancer is a type of head and neck tumor with a poor prognosis and survival rate. The new cases of laryngeal cancer increased rapidly with a higher mortality rate around the world.
The current research work was focused to unveil the antitumor effects of ononin against the laryngeal cancer Hep-2 cells.
The cytotoxic effects of ononin against the laryngeal cancer Hep-2 cells and normal HuLa-PC laryngeal cells were studied using an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The intracellular Reactive Oxygen Species (ROS) generation, apoptotic cell death, Mitochondrial Membrane Potential (MMP), and cell adhesion on the 25 and 50 µM ononin-treated Hep-2 cells were detected using respective staining assays. The levels of TBARS and antioxidants were assayed using specific kits. The expressions of c-Jun N-terminal kinase 1/2 (JNK1/2), Extracellular Signal-regulated Kinase 1/2 (ERK1/2), p38, Phosphatidylinositol-3 Kinase 1/2 (PI3K1/2), and protein kinase-B (Akt) in the ononin-treated Hep-2 cells were investigated using Reverse Transcription-Polymerase Chain Reaction (RT-PCR) assay.
The ononin treatment effectively inhibited the Hep-2 cell viability but did not affect the viability of HuLa-PC cells. Furthermore, the ononin treatment effectively improved the intracellular ROS accumulation, depleted the MMP, and triggered apoptosis in Hep-2 cells. The Thiobarbituric acid reactive substances (TBARS) were improved, and Glutathione (GSH) levels and Superoxide dismutase (SOD) were depleted in the ononin-administered Hep-2 cells. The ononin treatment substantially inhibited the JNK/ERK/p38 axis in the Hep-2 cells.
Together, the outcomes of this exploration proved that the ononin has remarkable antitumor activity against laryngeal cancer Hep-2 cells.
喉癌是一种头颈部肿瘤，预后和生存率较差。全球喉癌新发病例迅速增加，死亡率较高。
当前的研究工作聚焦于揭示鹰嘴豆芽素A对喉癌Hep-2细胞的抗肿瘤作用。
采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐（MTT）法研究鹰嘴豆芽素A对喉癌Hep-2细胞和正常HuLa-PC喉细胞的细胞毒性作用。使用相应的染色法检测25和50μM鹰嘴豆芽素A处理的Hep-2细胞内活性氧（ROS）的产生、凋亡细胞死亡、线粒体膜电位（MMP）和细胞黏附情况。使用特定试剂盒检测丙二醛（TBARS）和抗氧化剂水平。采用逆转录聚合酶链反应（RT-PCR）法研究鹰嘴豆芽素A处理的Hep-2细胞中c-Jun氨基末端激酶1/2（JNK1/2）、细胞外信号调节激酶1/2（ERK1/2）、p38、磷脂酰肌醇-3激酶1/2（PI3K1/2）和蛋白激酶B（Akt）的表达。
鹰嘴豆芽素A处理有效抑制了Hep-2细胞活力，但不影响HuLa-PC细胞活力。此外，鹰嘴豆芽素A处理有效促进了Hep-2细胞内ROS积累，降低了MMP，并引发细胞凋亡。在给予鹰嘴豆芽素A的Hep-2细胞中，硫代巴比妥酸反应物质（TBARS）升高，谷胱甘肽（GSH）水平和超氧化物歧化酶（SOD）降低。鹰嘴豆芽素A处理显著抑制了Hep-2细胞中的JNK/ERK/p38轴。
总之，本研究结果证明鹰嘴豆芽素A对喉癌Hep-2细胞具有显著的抗肿瘤活性。
