Stationed or Relocating: The Seesawing EMT/MET Determinants from Embryonic Development to Cancer Metastasis

Abstract

Epithelial and mesenchymal transition mechanisms continue to occur during the cell cycle and throughout human development from the embryo stage to death. In embryo development, epithelial-mesenchymal transition (EMT) can be divided into three essential steps. First, endoderm, mesoderm, and neural crest cells form, then the cells are subdivided, and finally, cardiac valve formation occurs. After the embryonic period, the human body will be subjected to ongoing mechanical stress or injury. The formation of a wound requires EMT to recruit fibroblasts to generate granulation tissues, repair the wound and re-create an intact skin barrier. However, once cells transform into a malignant tumor, the tumor cells acquire the characteristic of immortality. Local cell growth with no growth inhibition creates a solid tumor. If the tumor cannot obtain enough nutrition in situ, the tumor cells will undergo EMT and invade the basal membrane of nearby blood vessels. The tumor cells are transported through the bloodstream to secondary sites and then begin to form colonies and undergo reverse EMT, the so-called “mesenchymal-epithelial transition (MET).” This dynamic change involves cell morphology, environmental conditions, and external stimuli. Therefore, in this manuscript, the similarities and differences between EMT and MET will be dissected from embryonic development to the stage of cancer metastasis.

FOXM1-CD44 Signaling Is Critical for the Acquisition of Regorafenib Resistance in Human Liver Cancer Cells

“…EMT has been reported as one of the tumor-related functions that might enable the CSCs to gain the abilities of self-renewal and invasion and prevent apoptotic activity [ 32 , 33 , 34 ]. To understand the EMT phenomenon in regorafenib-resistant cells, we measured the expression of EMT marker genes using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) ( Figure 3 A).…”

“…EMT has been reported as one of the tumor-related functions that might enable the CSCs to gain the abilities of self-renewal and invasion and prevent apoptotic activity [32][33][34].…”

Possible Action of Olaparib for Preventing Invasion of Oral Squamous Cell Carcinoma In Vitro and In Vivo

“…This could be attributed to the differences in the extracellular matrix regarding collagen I and laminin [ 37 , 38 ], and the affinity between the extracellular matrix and each cell line. Moreover, considering that the process of MET is required for cells migrating to secondary sites to colonize metastatic regions [ 39 ], and genes increased in MET are reported to be E-cadherin and tight junction proteins [ 40 ], the results of the cell adhesion assay were supported by the significantly increased level of E-cadherin in Ca9-22 and HSC-2 cells ( Figure 5 ). The second most unexpected results were the result of cell proliferation assay, which showed suppressive effect six days after 1 µM olaparib exposure and SAS and HSC-2 cell lines did not reach confluence ( Figure 1 b,c).…”

NF‐κB as a regulator of cancer metastasis and therapy response: A focus on epithelial–mesenchymal transition

“…The epithelial cells are capable of generating barriers or they can separate spaces (C. H. Li et al, 2021). However, when this barrier is breached during pathological events such as injuries, the transformation of epithelial cells into fibroblast‐like cells occurs that is obvious from the morphology of cells (Ashrafizadeh, Zarrabi, Hushmandi, Kalantari et al, 2020; Rovensky Yu et al, 2001).…”