The EMT signaling pathways in endometrial carcinoma.
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.
Biomedical Research Unit, Vall d'Hebron Research Institute, Barcelona, Spain.
Eva
E
Colas
Nuria
N
Pedrola
Laura
L
Devis
Tugçe
T
Ertekin
Irene
I
Campoy
Elena
E
Martínez
Marta
M
Llauradó
Marina
M
Rigau
Mireia
M
Olivan
Marta
M
Garcia
Silvia
S
Cabrera
Antonio
A
Gil-Moreno
Jordi
J
Xercavins
Josep
J
Castellvi
Angel
A
Garcia
Santiago
S
Ramon y Cajal
Gema
G
Moreno-Bueno
Xavier
X
Dolcet
Francesc
F
Alameda
Jose
J
Palacios
Jaime
J
Prat
Andreas
A
Doll
Xavier
X
Matias-Guiu
Miguel
M
Abal
Jaume
J
Reventos
D002277:Carcinoma / Q000235:genetics / Q000473:pathology*; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000473:pathology; D016889:Endometrial Neoplasms / Q000235:genetics / Q000473:pathology*; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics* / Q000502:physiology; D005260:Female; D006801:Humans; D035683:MicroRNAs / Q000235:genetics / Q000502:physiology; D008954:Models, Biological; D009361:Neoplasm Invasiveness; D011980:Receptors, Progesterone / Q000235:genetics / Q000502:physiology; D015398:Signal Transduction / Q000235:genetics
D035683:MicroRNAs; D011980:Receptors, Progesterone