Open AccessBrief Report: The lincRNA Hotair Is Required for Epithelial‐to‐Mesenchymal Transition and Stemness Maintenance of Cancer Cell Lines
Author(s) -
Pádua Alves Cleidson,
Fonseca Aline Simoneti,
Muys Bruna Rodrigues,
Barros e Lima Bueno Rafaela,
Bürger Matheus Carvalho,
Souza Jorge E. S.,
Valente Valeria,
Zago Marco Antonio,
Silva Wilson Araújo
Publication year - 2013
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.1547
Subject(s) - hotair , biology , cancer stem cell , epithelial–mesenchymal transition , cancer research , cd44 , carcinogenesis , stem cell , prc2 , metastasis , epigenetics , chromatin , sox2 , long non coding rna , cancer , microbiology and biotechnology , cell , ezh2 , rna , transcription factor , genetics , gene
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. S tem C ells 2013;31:2827–2832