2. Academic Validation
  3. Ononin Shows Anticancer Activity Against Laryngeal Cancer via the Inhibition of ERK/JNK/p38 Signaling Pathway

Ononin Shows Anticancer Activity Against Laryngeal Cancer via the Inhibition of ERK/JNK/p38 Signaling Pathway

  • Front Oncol. 2022 Jul 14:12:939646. doi: 10.3389/fonc.2022.939646.
Ben Ye 1,  Jianhua Ma 2,  Zhaoxia Li 1,  Yang Li 3,  Xiaopan Han 4
Affiliations

Affiliations

  • 1 Department of Ear, Nose, and Throat (ENT), Shandong Provincial Hospital Affiliated to Shandong First Medical University, Ji'nan, China.
  • 2 Department of Cardiology, Shandong Rongjun General Hospital, Ji'nan, China.
  • 3 Department of Plastic Surgery, Central Hospital Affiliated to Shandong First Medical University, Jinan, China.
  • 4 Department of ENT, Central Hospital Affiliated to Shandong First Medical University, Ji'nan, China.
PMID: 35912256 DOI: 10.3389/fonc.2022.939646
Abstract

Background: 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.

Objective: The current research work was focused to unveil the in vitro antitumor effects of ononin against the laryngeal Cancer Hep-2 cells.

Methodology: 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.

Results: 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.

Conclusion: Together, the outcomes of this exploration proved that the ononin has remarkable antitumor activity against laryngeal Cancer Hep-2 cells.

Keywords

ERK/JNK/p38 pathway; Hep-2 cells; apoptosis; laryngeal cancer; ononin.

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