Amb motiu del tancament d'estiu, la validació de documents es reprendrà a partir del 28 d'agost de 2026. Disculpeu les molèsties.
Con motivo del cierre de verano, la validación de documentos se reanudará a partir del 28 de agosto de 2026. Disculpad las molestias
Due to the summer closure, document validation will resume starting August 28, 2026. We apologize for any inconvenience.

Document type

Article

Version

Accepted version

Publication date

All rights reserved

Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/167783

The EMT signaling pathways in endometrial carcinoma

Journal Title

Director/Tutor

Journal ISSN

Volume Title

Abstract

Endometrial cancer (EC) is the most common gynecologic malignancy of the female genital tract and the fourth most common neoplasia in women. In EC, myometrial invasion is considered one of the most important prognostic factors. For this process to occur, epithelial tumor cells need to undergo an epithelial to mesenchymal transition (EMT), either transiently or stably, and to differing degrees. This process has been extensively described in other types of cancer but has been poorly studied in EC. In this review, several features of EMT and the main molecular pathways responsible for triggering this process are investigated in relation to EC. The most common hallmarks of EMT have been found in EC, either at the level of E-cadherin loss or at the induction of its repressors, as well as other molecular alterations consistent with the mesenchymal phenotype-like L1CAM and BMI-1 up-regulation. Pathways including progesterone receptor, TGFβ, ETV5 and microRNAs are deeply related to the EMT process in EC.

Citation

Citation

COLÁS, Eva, et al. The EMT signaling pathways in endometrial carcinoma. Clinical & Translational Oncology. 2012. Vol. 14, num. 10, pags. 715-720. ISSN 1699-048X. [consulted: 18 of August of 2026]. Available at: https://hdl.handle.net/2445/167783

Export metadata

JSON - METS

Share record