Epithelial-to-Mesenchymal Transition in the Female Reproductive Tract: From Normal Functioning to Disease Pathology

被引:104
作者
Bilyk, Olena [1 ]
Coatham, Mackenzie [2 ]
Jewer, Michael [1 ,3 ]
Postovit, Lynne-Marie [1 ]
机构
[1] Univ Alberta, Dept Oncol, Edmonton, AB, Canada
[2] Univ Alberta, Dept Obstet & Gynecol, Edmonton, AB, Canada
[3] Western Univ, Dept Anat & Cell Biol, London, ON, Canada
基金
加拿大健康研究院;
关键词
epithelial-to-mesenchymal transition; adenomyosis; endometriosis; ovarian cancer; endometrial cancer; tumor microenvironment; OVARIAN-CANCER CELLS; NECROSIS-FACTOR-ALPHA; CIRCULATING TUMOR-CELLS; GRADE SEROUS OVARIAN; FOLLICLE-STIMULATING-HORMONE; INDUCIBLE FACTOR 1-ALPHA; ENDOMETRIAL CANCER; E-CADHERIN; TGF-BETA; FALLOPIAN-TUBE;
D O I
10.3389/fonc.2017.00145
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Epithelial-to-mesenchymal transition (EMT) is a physiological process that is vital throughout the human lifespan. In addition to contributing to the development of various tissues within the growing embryo, EMT is also responsible for wound healing and tissue regeneration later in adulthood. In this review, we highlight the importance of EMT in the development and normal functioning of the female reproductive organs (the ovaries and the uterus) and describe how dysregulation of EMT can lead to pathological conditions, such as endometriosis, adenomyosis, and carcinogenesis. We also summarize the current literature relating to EMT in the context of ovarian and endometrial carcinomas, with a particular focus on how molecular mechanisms and the tumor microenvironment can govern cancer cell plasticity, therapy resistance, and metastasis.
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页数:21
相关论文
共 259 条
[1]   Short-term single treatment of chemotherapy results in the enrichment of ovarian cancer stem cell-like cells leading to an increased tumor burden [J].
Abubaker, Khalid ;
Latifi, Ardian ;
Luwor, Rod ;
Nazaretian, Simon ;
Zhu, Hongjian ;
Quinn, Michael A. ;
Thompson, Erik W. ;
Findlay, Jock K. ;
Ahmed, Nuzhat .
MOLECULAR CANCER, 2013, 12
[2]  
Acs Geza, 2005, Am J Clin Pathol, V123 Suppl, pS13
[3]   Molecular pathways regulating EGF-induced epithelio-mesenchymal transition in human ovarian surface epithelium [J].
Ahmed, N ;
Maines-Bandiera, S ;
Quinn, MA ;
Unger, WG ;
Dedhar, S ;
Auersperg, N .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2006, 290 (06) :C1532-C1542
[4]   Epithelial-mesenchymal interconversions in normal ovarian surface epithelium and ovarian carcinomas: An exception to the norm [J].
Ahmed, Nuzhat ;
Thompson, Erik W. ;
Quinn, Michael A. .
JOURNAL OF CELLULAR PHYSIOLOGY, 2007, 213 (03) :581-588
[5]   Getting to know ovarian cancer ascites: opportunities for targeted therapy-based translational research [J].
Ahmed, Nuzhat ;
Stenvers, Kaye L. .
FRONTIERS IN ONCOLOGY, 2013, 3
[6]   Molecular profiling of circulating tumor cells links plasticity to the metastatic process in endometrial cancer [J].
Alonso-Alconada, Lorena ;
Muinelo-Romay, Laura ;
Madissoo, Kadri ;
Diaz-Lopez, Antonio ;
Krakstad, Camilla ;
Trovik, Jone ;
Wik, Elisabeth ;
Hapangama, Dharani ;
Coenegrachts, Lieve ;
Cano, Amparo ;
Gil-Moreno, Antonio ;
Chiva, Luis ;
Cueva, Juan ;
Vieito, Maria ;
Ortega, Eugenia ;
Mariscal, Javier ;
Colas, Eva ;
Castellvi, Josep ;
Cusido, Maite ;
Dolcet, Xavier ;
Nijman, Hans W. ;
Bosse, Tjalling ;
Green, John A. ;
Romano, Andrea ;
Reventos, Jaume ;
Lopez-Lopez, Rafael ;
Salvesen, Helga B. ;
Amant, Frederic ;
Matias-Guiu, Xavier ;
Moreno-Bueno, Gema ;
Abal, Miguel .
MOLECULAR CANCER, 2014, 13
[7]   Genes of glycolysis are ubiquitously overexpressed in 24 cancer classes [J].
Altenberg, B ;
Greulich, KO .
GENOMICS, 2004, 84 (06) :1014-1020
[8]   Micro-RNA signature of the epithelial-mesenchymal transition in endometrial carcinosarcoma [J].
Angeles Castilla, Maria ;
Moreno-Bueno, Gema ;
Romero-Perez, Laura ;
Van De Vijver, Koen ;
Biscuola, Michele ;
Angeles Lopez-Garcia, Maria ;
Prat, Jaime ;
Matias-Guiu, Xavier ;
Cano, Amparo ;
Oliva, Esther ;
Palacios, Jose .
JOURNAL OF PATHOLOGY, 2011, 223 (01) :72-80
[9]  
[Anonymous], END ABSTR
[10]  
[Anonymous], AACR SPEC C ADV OV C