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Placa J.R.,National Institute of Science and Technology in Stem Cell | Placa J.R.,University of Sao Paulo | Bueno R.D.B.E.L.,University of Sao Paulo | Bueno R.D.B.E.L.,National Institute of Science and Technology in Stem Cell | And 8 more authors.
Genomics Data | Year: 2015

Laryngeal squamous cell carcinoma (LSCC) is one of the most common malignancies of the head and neck tumors Zhang et al., 2013 [1]). Previous studies have associated its occurrence with social activities, such as tobacco and alcohol consumption (Hashibe et al., 2007a [2]; Hashibe et al., 2007b [3]; Shangina et al., 2006 [4]). Here, we performed a genome-wide gene expression profiling in thirty-one patients positively diagnosed for LSCC, in order to investigate new targets involved in tumorigenesis. © 2015.


Alves C.P.,Centro Regional Of Hemoterapia Of Ribeirao Preto | Alves C.P.,National Institute of Science and Technology in Stem Cell | Alves C.P.,University of Sao Paulo | Fonseca A.S.,Centro Regional Of Hemoterapia Of Ribeirao Preto | And 21 more authors.
Stem Cells | Year: 2013

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-b1 resulted in increased Hotair expression and triggered the EMT program. Interestingly, ablation of Hotair expression by siRNA prevented the EMT program stimulated by TGF-b1, and also the colony-forming capacity of colon and breast cancer cells. Furthermore, we observed that the colon CSC subpopulation (CD1331/CD441) 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. © AlphaMed Press.

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