Tumors are cellularly and molecularly heterogeneous, with subsets of 
undifferentiated cancer cells exhibiting stem cell-like features (CSCs). 
Epithelial to mesenchymal transitions (EMT) are transdifferentiation programs 
that are required for tissue morphogenesis during embryonic development. The EMT 
process can be regulated by a diverse array of cytokines and growth factors, 
such as transforming growth factor (TGF)-beta, whose activities are dysregulated 
during malignant tumor progression. Thus, EMT induction in cancer cells results 
in the acquisition of invasive and metastatic properties. Recent reports 
indicate that the emergence of CSCs occurs in part as a result of EMT, for 
example, through cues from tumor stromal components. Recent evidence now 
indicates that EMT of tumor cells not only causes increased metastasis, but also 
contributes to drug resistance. In this review, we will provide potential 
mechanistic explanations for the association between EMT induction and the 
emergence of CSCs. We will also highlight recent studies implicating the 
function of TGF-beta-regulated noncoding RNAs in driving EMT and promoting CSC 
self-renewal. Finally we will discuss how EMT and CSCs may contribute to drug 
resistance, as well as therapeutic strategies to overcome this clinically.