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LONG NON‐CODING RNA HOTAIR ACTIVATION BY TGF‐BETA1 INDUCES EPITHELIAL MESENCHYMAL TRANSITION (EMT) IN T24 BLADDER CARCINOMA CELLS
Author(s) -
Oliveira Brito Rodrigo Barbosa,
Malta Camila Soares,
Matos Yves Silva Teles,
Souza Diego Mota,
Matheus Luiz Henrique Gomes,
Dalboni Maria Aparecida,
Dellê Humberto
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.439.7
Subject(s) - hotair , epithelial–mesenchymal transition , cancer research , long non coding rna , metastasis , twist transcription factor , transforming growth factor , mesenchymal stem cell , cadherin , downregulation and upregulation , bladder cancer , cell , chemistry , biology , cancer , medicine , gene , microbiology and biotechnology , biochemistry
HOTAIR is a long non‐coding RNA (lncRNA) which is implicated in cell programming for initiation of epithelial mesenchymal transition (EMT) in several types of cancer. In bladder carcinoma T24 cells, the TGF‐beta1 promotes invasion and metastasis through induction of EMT, however, there are evidences to believe that HOTAIR is a possible link between TGF‐beta1 and EMT in bladder cancer. The aim of this study was to analyze the expression of IncRNA HOTAIR in human bladder carcinoma T24 cells incubated with TGF‐beta1, in order to correlate it with markers for EMT. Bladder carcinoma cells (T24) were incubated with TGF‐beta1 (5 ng/ml) during 48h and then total RNA was extract to analyze the expression of Hotair, N‐cadherin (nCAD, a mesenchymal cell marker), E‐cadherin (eCAD, an epithelial cell marker), and Twist (an EMT transcription factor) by RT‐qPCR. The results are presented in mean±SEM, considering relative expression (RE). T24 cells stimulated with TGF‐beta1 presented an increased Hotair expression (RE 2.80 ± 0.14 vs. 1.00 ± 0.17 in control, p<0.001). TGF‐beta1 upregulated the expression of nCAD gene (RE 2.22 ± 0.55 vs 1.00 ± 0.32 in control, p <0.0001), while decreased eCAD expression (RE 0.23 ± 0.15 vs 1.00 ± 0.07 in control, p <0.05). The Twist expression was significantly increased by treatment with TGF‐beta1 (RE 3.05 ± 0.54 vs 1.00 ± 0.32 in control, p <0.001). We conclude that TGF‐beta1 upregulates Hotair expression in T24 cells, correlating with the EMT. It is possible that HOTAIR is involved in cell invasion and metastasis in bladder cancer. Support or Funding Information FAPESP (2012/04423‐0)