Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2012 Oct;14(10):715-20.
doi: 10.1007/s12094-012-0866-3. Epub 2012 Aug 22.

The EMT signaling pathways in endometrial carcinoma

Affiliations
Free article
Review

The EMT signaling pathways in endometrial carcinoma

Eva Colas et al. Clin Transl Oncol. 2012 Oct.
Free article

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.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Gynecol Oncol. 1983 Feb;15(1):10-7 - PubMed
    1. J Pathol. 2005 Dec;207(4):422-9 - PubMed
    1. Nat Rev Cancer. 2004 Nov;4(11):839-49 - PubMed
    1. Nat Rev Mol Cell Biol. 2006 Feb;7(2):131-42 - PubMed
    1. J Pathol. 2003 Apr;199(4):471-8 - PubMed

Publication types

MeSH terms

-