EMT can also be seen as a reversible transdifferentiation program whereby non-motile epithelial cells transform into migratory mesenchymal cells with enhanced cell survival attributes. This transformation is recognized by a loss of epithelial nature, followed by an increase in mesenchymal markers such as N-cadherin and vimentin (112-114).

A battery of critical transcriptional factors like SNAI1, SNAI2, ZEB1, ZEB2, Twist, as well as several lncRNA (long non-coding RNAs) through the complex chromatin remodeling process, brings about epigenetic modifications that drive the EMT process. Signaling from most of these pathways converges to repress the expression of epithelial marker E-cadherin, regarded as a ‘master’ regulator of EMT. Loss of E-cadherin gene somatically is found in several cancers such as breast cancer, gastric carcinoma. This is often associated with loss of epithelial characteristics and [?]

2. INTRODUCTION

Trophoblast cells are derived from the outer trophoectodermal layer of the developing blastocysts as a part of the outer cell mass that eventually forms the placenta (1). These cells help in establishing cell to cell interactions that eventually secure and anchor the blastocysts into the uterus (2).

In humans, the blastocyst “hatches” out of the protective zona pellucida approximately after five days, which facilitates the blastocyst adhesion to the uterine endometrium, thereby gaining access to the maternal cytokine and nutrient milieu (3). Through a process called zona hatching, the embryo is released from the blastocyst. The cells on the outer side of blastocyst become trophectoderm, which differentiates into chorion, forming the future placenta while the inner cell mass becomes the embryo. This process is the first step towards embryogenesis and often subjected to precision control both by the maternal as well as embryonic factors.