Backgrounds: Excessive pepsin can damage both normal laryngeal epithelial cells and laryngeal cancer (LC) cells. unc-51-like kinase 1 (ULK1) is closely related to endoplasmic reticulum stress (ERS). In this paper, we will explore the different significance of the regulatory role of ULK1 in ERS level in pepsin-treated laryngeal epithelial cells and LC cells.
Methods: In cell experiments, laryngeal epithelial cells and LC cells were selected and induced by different concentrations of pepsin. Cell activity was detected by CCK8, cell apoptosis was detected by flow cytometry. The expression of ER-related proteins was detected by Western blot. Cell transfection was used to inhibit ULK1 expression in both cells, and ERS, apoptosis, were measured using related techniques.
Results: ULK1 was increased in pepsin-stimulated laryngeal epithelial cells and LC cells, thereby increasing ER and ER-induced apoptosis and cell proliferation. Inhibition of ULK1 reduced the expression of ER-related proteins in pepsin-stimulated laryngeal epithelial cells and LC cells.
Conclusion: ER level regulated by ULK1 had different significance in laryngeal epithelial cells and LC cells treated with pepsin.
Yujie Feng, Ph.D Student, Department of Voice, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, 361102, Xiamen, China.
Peiyun Zhuang, M.S, Professor, Director, Department of Voice, Zhongshan Hospital Xiamen University, Xiamen 361002, China