N‑glycosylation and receptor tyrosine kinase signaling affect claudin‑3 levels in colorectal cancer cells.

ABSTRACT: Changes in protein levels in different components of the apical junctional complex occur in colorectal cancer (CRC). Claudin‑3 is one of the main constituents of tight junctions, and its overexpression can increase the paracellular flux of macromolecules, as well as the malignant potential of CRC cells. The aim of this study was to investigate the molecular mechanisms involved in the regulation of claudin‑3 and its prognostic value in CRC. In silico evaluation in each of the CRC consensus molecular subtypes (CMSs) revealed that high expression levels of CLDN3 (gene encoding claudin‑3) in CMS2 and CMS3 worsened the patients' long‑term survival, whereas a decrease in claudin‑3 levels concomitant with a reduction in phosphorylation levels of epidermal growth factor receptor (EGFR) and insulin

SUBMITTER: Perez AG 

PROVIDER: S-EPMC7448416 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature