ABCB5: ATP-binding cassette sub-family B member 5; ABCG2: ATP-binding
cassette sub-family G member 2; ALDH1: aldehyde dehydrogenase 1A1; Bmi1:
B cell-specific Moloney murine leukemia virus integration site 1; CD24:
heat stable antigen; CD34: hematopoietic progenitor cell antigen; CD38:
cyclic ADP ribose hydrolase; CD44: hyaluronate receptor; CD90: Thymocyte
differentiation antigen-1; CD133: prominin-1; CD117: c-kit ; CSC: cancer
stem cell; CXCR4: receptor for chemokine; EpCAM: epithelial cell
adhesion molecule; ESA: epithelial surface antigen
Tumorigenesis has been explained by two different models, namely the
stochastic model and the hierarchical model (CSC model). According to
stochastic model, transformation of somatic cells leads to generation of
tumor. In contrast, the hierarchical model states that CSCs are the
origin of tumor formation (Barbato et al., 2019; Batlle &
Clevers, 2017) . CSCs can themselves be derived clonally via cell
division (symmetric or asymmetric) of cancer progenitor cells or
transformed stem cells (Oh et al., 2016) . Overall, CSCs give
rise to aggressively metastasizing tumors.
Tumor cells are known to undergo phenotypic alteration as a consequence
of EMT during cancer progression. In EMT, the epithelial cells develop
the traits of mesenchymal cells which is characterized by E-cadherin
downregulation and N-cadherin upregulation, which in turn is regulated
by numerous transcription factors such as Snail, Slug and Twist(Nistico et al., 2012; Salehi et al., 2019, Sinha et al.,
2019) . EMT causes the apical-basal polar epithelial cells to depict
front-rear polarity of mesenchymal cells, due to which they show
enhanced motility and migration properties (Antony et al.,
2019) .