Amygdalin Induced Mitochondria-Mediated Apoptosis of Hypopharyngeal Carcinoma

Abstract

Purpose: Amygdalin is a natural extract effective in cancer inhibition, though its effects on hypopharyngeal squamous cell carcinoma (HSCC) have not been investigated. This study aims to investigate the in vitro anti-hypopharyngeal carcinoma activity of amygdalin and its potential mechanism. Methods: The hypopharyngeal squamous cell carcinoma cell lines (FADU and TU212) were treated with amygdalin. The proliferation of hypopharyngeal carcinoma was tested by mitochondria targeting sequence (MTS) assay. Furthermore, Annexin V-fluorescein isothiocyanate/propidine iodide (Annexin V-FITC/PI) double staining, immunofluorescence and mitochondrial membrane potential (MMP) assays were taken to test apoptosis. Apoptotic mRNA transcript levels and protein expression were evaluated using real-time quantitative PCR (qPCR) and western blot (WB). Results: FADU and TU212 cells were treated with amygdalin. MTS assay showed that amygdalin inhibited the proliferation of hypopharyngeal carcinoma cells. Annexin V-FITC/PI double staining, immunofluorescence and MMP detection assays were carried out and confirmed that amygdalin induced apoptosis in hypopharyngeal carcinoma cells. In addition, qPCR and WB analysis suggested that amygdalin exerted a carcinogenic anti-hypopharyngeal effect by mediating the mitochondrial apoptosis pathway. Conclusions: Amygdalin can inhibit the proliferation of hypopharyngeal carcinoma cells and promote apoptosis of hypopharyngeal carcinoma cells by inducing the mitochondrial apoptosis pathway. Amygdalin is a potential chemotherapeutic agent for hypopharyngeal carcinoma.