EMT is also associated with loss of E-cadherin, SNAIL, Twist and activation of β-catenin gene expression which make cells lose their adhesion and facilitate metastasis[32]. INK 128 structure However, some studies claim that the process of EMT is only observed in ATC.

Authors have scripted the role of microRNAs in this transition process which makes CSCs undergo unlimited proliferation and capable of initiating tumor growth at metastatic sites[10,25,31]. However, this area needs to be further explored before designing therapies aimed at the eradication of transformed cells. In an attempt to develop targeted therapeutic strategies to eradicate this subset of CSCs, it becomes essential to determine their origin and whether they differ in various sub-types of thyroid cancer. Studies have shown overexpressed multi-drug resistance protein 1 (MDR 1) and ABCG2 transporters to cause resistance to cytotoxic drugs. With this concept, Zheng et al[32] displayed how doxorubicin becomes ineffective and fail to eradicate CSC population. Because these drugs can specifically kill cancer cells, it provides a major space for CSCs to proliferate making the tumor resistant to chemotherapy, thus causing the disease to relapse[32] (Figure ​(Figure44). Figure 4 A schematic representation showing cancer stem cells resistance to chemo-and radio-therapy causing

tumor to relapse. Cancer stem cells (CSCs) (yellow) with differentiated cells committed to a particular lineage (red). Ability of CSCs to resist anti-cancer … In conclusion, therapeutic rationale should be laid, specifically, on destruction of CSCs by abruption of self-renewal signaling pathways, induction of differentiation of cancer cells and inhibition of survival-related mechanisms. Another venue to develop specific targeted therapies is by identification and destruction of the niche that nourishes CSCs for tumor growth. Because CSCs are heterogeneous and the cell-specific markers vary enormously amongst different tumor-types, GSK-3 there is an urgent need to

identify further specific markers to support their existence. Further advancements in stem cell technology should focus on conglomerated existence of factors responsible for failure of current therapies in eradicating thyroid CSCs with the aim to target specific subpopulation of cells in the patients with refractory thyroid cancers. Footnotes P- Reviewer: Li CJ, Zoller M S- Editor: Tian YL L- Editor: A E- Editor: Lu YJ
Core tip: Genome-wide alterations in gene expression in human pluripotent stem cells (hPSCs) following genotoxic stress exposures may underlie the ultimate fate and outcome of practical utility of hPSCs which makes systematic studies of these effects a high priority in stem cell research.