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Chunk #14 — RESULTS — CtBP2 acted as a transcriptional co-repressor and its recruitment was critical for GLI1/SNAI1 induction of the HCC EMT phenotype

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CtBP2 is an independent prognostic marker that promotes GLI1 induced epithelial-mesenchymal transition in hepatocellular carcinoma.
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To investigate whether CtBP2 directly induced EMT, we examined the relationship between CtBP2, SNAI1 and EMT in HCC. We abolished SNAI1 expression in Huh7 cells using SNAI1 siRNA [21] and induced CtBP2 expression with transfection of a CtBP2 expressing plasmid (Figure 6A). In the absence of SNAI1, CtBP2 overexpression did not affect the expression of E-cadherin, N-cadherin, Vimentin or Fibronectin as much as it did in cells expressing normal levels of SNAI1, as presented in Figure 6B. This result indicated that SNAI1 was required for CtBP2-driven EMT and that CtBP2 was not a direct mediator of EMT in HCC.