Hotair is a member of the recently described class of noncoding RNAs called 
lincRNA (large intergenic noncoding RNA). Various studies suggest that Hotair 
acts regulating epigenetic states by recruiting chromatin-modifying complexes to 
specific target sequences that ultimately leads to suppression of several genes. 
Although Hotair has been associated with metastasis and poor prognosis in 
different tumor types, a deep characterization of its functions in cancer is 
still needed. Here, we investigated the role of Hotair in the scenario of 
epithelial-to-mesenchymal transition (EMT) and in the arising and maintenance of 
cancer stem cells (CSCs). We found that treatment with TGF-β1 resulted in 
increased Hotair expression and triggered the EMT program. Interestingly, 
ablation of Hotair expression by siRNA prevented the EMT program stimulated by 
TGF-β1, and also the colony-forming capacity of colon and breast cancer cells. 
Furthermore, we observed that the colon CSC subpopulation (CD133(+)/CD44(+)) 
presents much higher levels of Hotair when compared with the non-stem cell 
subpopulation. These results indicate that Hotair acts as a key regulator that 
controls the multiple signaling mechanisms involved in EMT. Altogether, our data 
suggest that the role of Hotair in tumorigenesis occurs through EMT triggering 
and stemness acquisition.