Advanced search
Start date
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Brief Report: The lincRNA Hotair Is Required for Epithelial-to-Mesenchymal Transition and Stemness Maintenance of Cancer Cell Lines

Full text
Alves, Cleidson Padua [1, 2, 3, 4] ; Fonseca, Aline Simoneti [1, 2, 3] ; Muys, Bruna Rodrigues [1, 2, 3] ; Bueno, Rafaela de Barros e Lima [1, 2, 3] ; Buerger, Matheus Carvalho [5, 1, 2, 3, 4] ; de Souza, Jorge E. S. [5, 1, 2, 3, 4] ; Valente, Valeria [1, 3, 4, 6] ; Zago, Marco Antonio [1, 3, 7] ; Silva, Jr., Wilson Araujo [1, 2, 3, 4]
Total Authors: 9
[1] Natl Inst Sci & Technol Stem Cell & Cell Therapy, Sao Paulo - Brazil
[2] Univ Sao Paulo, Dept Genet, Ribeirao Preto Med Sch, Sao Paulo - Brazil
[3] Ctr Cell Based Therapy, Sao Paulo - Brazil
[4] Univ Sao Paulo, Ctr Integrat Syst Biolo CISBi, NAP, BR-09500900 Sao Paulo - Brazil
[5] Inst Bioinformat & Biotechnol 2bio, Sao Paulo - Brazil
[6] Univ Estadual Paulista, Fac Pharmaceut Sci Araraquara, Sao Paulo - Brazil
[7] Univ Sao Paulo, Dept Internal Med, Ribeirao Preto Med Sch, Sao Paulo - Brazil
Total Affiliations: 7
Document type: Journal article
Source: Stem Cells; v. 31, n. 12, p. 2827-2832, DEC 2013.
Web of Science Citations: 115

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-1 resulted in increased Hotair expression and triggered the EMT program. Interestingly, ablation of Hotair expression by siRNA prevented the EMT program stimulated by TGF-1, 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. (AU)

FAPESP's process: 98/14247-6 - Center for Research on Cell-Based Therapy
Grantee:Marco Antonio Zago
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC