Pepsin promotes IL-8 signaling-induced epithelial-mesenchymal transition in laryngeal carcinoma.

ABSTRACT:

Background

Laryngopharyngeal reflux (LPR), with its increasing morbidity, is attracting considerable attention. In recent years, the causal role between LPR and laryngeal carcinoma has been debated. The main harmful component of LPR is pepsin, which has been shown to induce mucosal inflammation by damaging the mucous membrane. Thus, pepsin is linked to an increased risk of laryngeal carcinoma, although the potential mechanism remains largely unknown.

Methods

The human laryngeal carcinoma cell lines Hep-2 and Tu212 were exposed to different pepsin concentrations and the morphology, proliferation, migration, secretion of inflammatory cytokines, and epithelial-mesenchymal transition (EMT) of the cells were assessed. To evaluate whether interleukin-8 (IL-8) had a causal relation

SUBMITTER: Tan JJ 

PROVIDER: S-EPMC6425698 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature