E-cadherin variants associated with oral facial clefts trigger aberrant cell motility in a REG1A-dependent manner.

ABSTRACT:

Background

Germline mutations of E-cadherin contribute to hereditary diffuse gastric cancer (HDGC) and congenital malformations, such as oral facial clefts (OFC). However, the molecular mechanisms through which E-cadherin loss-of-function triggers distinct clinical outcomes remain unknown. We postulate that E-cadherin-mediated disorders result from abnormal interactions with the extracellular matrix and consequent aberrant intracellular signalling, affecting the coordination of cell migration.

Methods

Herein, we developed in vivo and in vitro models of E-cadherin mutants associated with either OFC or HDGC. Using a Drosophila approach, we addressed the impact of the different variants in cell morphology and migration ability. By combining gap closure migration assays and time

SUBMITTER: Pereira J 

PROVIDER: S-EPMC10898076 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature