Studies on the expression of a novel splice variant of human E-cadherin in Endometrial Cancer

GIL-MORENO ANTONIO; ROSSO MARINA; VAZQUEZ-LEVIN MÓNICA HEBE; COLÁS EVA; MATOS MARÍA LAURA; JAUME REVENTOS; LARA LAPYCKYJ; BESSO MARIA JOSE

Congreso; Reunión Conjunta de Biociencias; 2017

Endometrial cancer (EC) is the 6th most common cancer in women worldwide. Endometrioid Endometrial Carcinomas (EEC) are ~80% of EC cases. Myometrial invasion (MI) is a key event in EC dissemination and deep MI is critical to define EC recurrence risk and associated with poor prognosis. Epithelial Cadherin (Ecad)-mediated cell-cell adhesion is altered, and Epithelial to Mesenchymal Transition (EMT)-related events occur during tumor progression in EEC, but the molecular basis are not fully known. We have identified a novel E-cadherin splice variant (Ecadvar) mRNA that induces an EMT phenotype in a breast cancer model. The present study aims to evaluate Ecadvar mRNA expression levels in EEC.Materials & Methods: QRT-PCR assays were run to quantify Ecadvar expression relative to Ecadwt in (A) In vitro studies with Hec1a cells (A1) stably transfected with ETV5 transcription factor, found in the invasive front of EC, (A2) treated with TGF-β1, a cytokine that induces EMT, (A3) transiently transfected with Ecad siRNA to downregulate the wild type Ecad. (B) Tissue endometrial biopsies from EC patients and controls.Results: (A1) Hec1a-ETV5 cells showed higher (p