The EMT signaling pathways in endometrial carcinoma

Eva Colas; Nuria Pedrola; Laura Devis; Tugçe Ertekin; Irene Campoy; Elena Martínez; Marta Llauradó; Marina Rigau; Mireia Olivan; Marta Garcia; Silvia Cabrera; Antonio Gil-Moreno; Jordi Xercavins; Josep Castellvi; Angel Garcia; S. Santiago Ramon Y Cajal; Gema Moreno-Bueno; Xavier Dolcet; Francesc Alameda; Jose Palacios; Jaime Prat; Andreas Doll; Xavier Matias-Guiu; Miguel Abal; Jaume Reventos

doi:10.1007/s12094-012-0866-3

The EMT signaling pathways in endometrial carcinoma

Eva Colas, Nuria Pedrola, Laura Devis, Tugçe Ertekin, Irene Campoy, Elena Martínez, Marta Llauradó, Marina Rigau, Mireia Olivan, Marta Garcia, Silvia Cabrera, Antonio Gil-Moreno, Jordi Xercavins, Josep Castellvi, Angel Garcia, S. Santiago Ramon Y Cajal, Gema Moreno-Bueno, Xavier Dolcet, Francesc Alameda, Jose PalaciosJaime Prat, Andreas Doll, Xavier Matias-Guiu, Miguel Abal, Jaume Reventos

Research output: Contribution to journal › Review article › Research › peer-review

84 Citations (Scopus)

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. © Federación de Sociedades Españolas de Oncología (FESEO) 2012.

Original language	English
Pages (from-to)	715-720
Journal	Clinical and Translational Oncology
Volume	14
Issue number	10
DOIs	https://doi.org/10.1007/s12094-012-0866-3
Publication status	Published - 1 Oct 2012

Keywords

EMT
Endometrial cancer
Invasion

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1007/s12094-012-0866-3

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Colas, E., Pedrola, N., Devis, L., Ertekin, T., Campoy, I., Martínez, E., Llauradó, M., Rigau, M., Olivan, M., Garcia, M., Cabrera, S., Gil-Moreno, A., Xercavins, J., Castellvi, J., Garcia, A., Santiago Ramon Y Cajal, S., Moreno-Bueno, G., Dolcet, X., Alameda, F., ... Reventos, J. (2012). The EMT signaling pathways in endometrial carcinoma. Clinical and Translational Oncology, 14(10), 715-720. https://doi.org/10.1007/s12094-012-0866-3

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title = "The EMT signaling pathways in endometrial carcinoma",

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. {\textcopyright} Federaci{\'o}n de Sociedades Espa{\~n}olas de Oncolog{\'i}a (FESEO) 2012.",

keywords = "EMT, Endometrial cancer, Invasion",

author = "Eva Colas and Nuria Pedrola and Laura Devis and Tug{\c c}e Ertekin and Irene Campoy and Elena Mart{\'i}nez and Marta Llaurad{\'o} and Marina Rigau and Mireia Olivan and Marta Garcia and Silvia Cabrera and Antonio Gil-Moreno and Jordi Xercavins and Josep Castellvi and Angel Garcia and {Santiago Ramon Y Cajal}, S. and Gema Moreno-Bueno and Xavier Dolcet and Francesc Alameda and Jose Palacios and Jaime Prat and Andreas Doll and Xavier Matias-Guiu and Miguel Abal and Jaume Reventos",

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Colas, E, Pedrola, N, Devis, L, Ertekin, T, Campoy, I, Martínez, E, Llauradó, M, Rigau, M, Olivan, M, Garcia, M, Cabrera, S , Gil-Moreno, A, Xercavins, J, Castellvi, J, Garcia, A, Santiago Ramon Y Cajal, S, Moreno-Bueno, G, Dolcet, X, Alameda, F, Palacios, J, Prat, J, Doll, A, Matias-Guiu, X, Abal, M & Reventos, J 2012, 'The EMT signaling pathways in endometrial carcinoma', Clinical and Translational Oncology, vol. 14, no. 10, pp. 715-720. https://doi.org/10.1007/s12094-012-0866-3

TY - JOUR

T1 - The EMT signaling pathways in endometrial carcinoma

AU - Colas, Eva

AU - Pedrola, Nuria

AU - Devis, Laura

AU - Ertekin, Tugçe

AU - Campoy, Irene

AU - Martínez, Elena

AU - Llauradó, Marta

AU - Rigau, Marina

AU - Olivan, Mireia

AU - Garcia, Marta

AU - Cabrera, Silvia

AU - Gil-Moreno, Antonio

AU - Xercavins, Jordi

AU - Castellvi, Josep

AU - Garcia, Angel

AU - Santiago Ramon Y Cajal, S.

AU - Moreno-Bueno, Gema

AU - Dolcet, Xavier

AU - Alameda, Francesc

AU - Palacios, Jose

AU - Prat, Jaime

AU - Doll, Andreas

AU - Matias-Guiu, Xavier

AU - Abal, Miguel

AU - Reventos, Jaume

PY - 2012/10/1

Y1 - 2012/10/1

N2 - 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. © Federación de Sociedades Españolas de Oncología (FESEO) 2012.

AB - 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. © Federación de Sociedades Españolas de Oncología (FESEO) 2012.

KW - EMT

KW - Endometrial cancer

KW - Invasion

U2 - 10.1007/s12094-012-0866-3

DO - 10.1007/s12094-012-0866-3

M3 - Review article

VL - 14

SP - 715

EP - 720

IS - 10

ER -

The EMT signaling pathways in endometrial carcinoma

Abstract

Keywords

UN SDGs

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