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) .