The regulatory mechanism of HSP70 in endoplasmic reticulum stress in pepsin-treated laryngeal epithelium cells and laryngeal cancer cells

Abstract

Backgrounds: Excessive pepsin can damage both normal laryngeal epithelial cells and laryngeal cancer (LC) cells. Heat shock protein 70 (HSP70) is closely related to pepsin. In this paper, we will explore the different significance of the regulatory role of HSP70 in endoplasmic reticulum stress (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, and autophagy was detected by autophagy detection kit. The expression of ER)-related proteins was detected by immunofluorescence (IF) and Western blot. Cell transfection was used to inhibit HSP70 expression in both cells, and ERS, apoptosis, and autophagy were measured using related techniques. In animal experiments, a mouse model bearing LC was established. TUNEL assay detected apoptosis, autophagy kit detected autophagy, and ER-related protein expression was detected by Western blot. Results: HSP70 was increased in pepsin-stimulated laryngeal epithelial cells and LC cells, thereby inhibiting ER and ER-induced apoptosis and autophagy. Inhibition of HSP70 reduced the expression of glucose regulated protein 78 (GRP78) in pepsin-stimulated laryngeal epithelial cells and LC cells, and only inhibited downstream apoptosis-related pathways in laryngeal epithelial cells rather than in LC cells. Inhibition of HSP70 and ER could significantly promote apoptosis and inhibit tumor growth in the absence of pepsin stimulation in vivo. Conclusion: ER level regulated by HSP70 had different significance in laryngeal epithelial cells and LC cells treated with pepsin.

SOAT1 in gallbladder cancer: Clinicopathological significance and avasimibe therapeutics

“…[71] Inducing ERS to promote cancer cell apoptosis has emerged as a novel anticancer treatment method. [72,73] This research investigates the role of SOAT1 in GBC patient cell lines and tissues, examining its relationship with clinicopathological features and survival outcomes. The project introduces avasimibe, a specific SOAT1 inhibitor, to explore its effects on GBC cellular behaviors, including proliferation, migration, invasion, and apoptosisrelated protein levels.…”

“…[ 71 ] Inducing ERS to promote cancer cell apoptosis has emerged as a novel anticancer treatment method. [ 72,73 ]…”

Pepsin Inhibitors Prevent Inflammation and Loss of Laryngeal Barrier Function in Mice with Gastroesophageal Reflux

“…2,16 Its mechanism of cell injury has been recently reported to be associated with a decreased expression in the E-cadherin junction protein, 17 increased expression of interleukin-8 (IL-8) by the CXRC2 18 receptor, decreased expression of carbonic anhydrase III (CA III), 14 and decreased expressions sep70 and sep53. 19 It also potentiates the regulatory mechanism of heat shock proteins 70 (HSP70) in the endoplasmic reticulum, 19,20 increases mucin 5 AC mRNA levels, induces NFKb activation, 21 and promotes oxidative 22 and mucosal damage. 9 Furthermore, pepsin has also been reported as a gastric aspiration marker associated with GERD.…”