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Review
. 2017 Jul 5:7:145.
doi: 10.3389/fonc.2017.00145. eCollection 2017.

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

Affiliations
Review

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

Olena Bilyk et al. Front Oncol. .

Abstract

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.

Keywords: adenomyosis; endometrial cancer; endometriosis; epithelial-to-mesenchymal transition; ovarian cancer; tumor microenvironment.

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Figures

Figure 1
Figure 1
Representative diagram of epithelial-to-mesenchymal transition (EMT)/mesenchymal-to-epithelial transition (MET) in female reproductive tract. EMT/MET are highly regulated physiological processes in embryo implantation and early development as well as in the reproductive function of the ovary and endometrium. Dysfunction of EMT in the normal epithelial cells of the ovary and uterus results in pathological processes, such as adenomyosis, endometriosis, cancer initiation, progression, and resistance to therapy. OSE, ovarian surface epithelium; LG serous OC, low-grade serous ovarian cancer; HG OC, high-grade ovarian cancer; FT epithelium, fallopian tube epithelium; EC, endometrial cancer. For a detailed description of the diagram and references refer to Sections “Physiological (Non-Malignant) EMT in the Female Reproductive Tract” and “EMT in Cancers of the Female Reproductive Tract.”
Figure 2
Figure 2
Epithelial-to-mesenchymal transition (EMT) in ovarian and endometrial cancers (ECs). Regulation of EMT-inducing signaling pathways through autocrine–paracrine signaling, chemotherapy, increased glycolysis, and the action of microRNAs. For a detailed description of the diagram and references refer to Sections “EMT in the Female Reproductive Tract,” “Molecular Mechanisms Governing EMT in Ovarian and ECs,” and “Microenvironmental Regulation of EMT in Cancers of the Female Reproductive Tract.”

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