Figure 7
AMOT-p80 rescues the phenotype seen on knockdown of HOXD10 and is highly expressed in primary HNSCC. (A) Expression of AMOT assessed using qPCR and WB, confirming reduced expression in the HOXD10 shRNA stably transfected cells, and increased expression in AMOT-p80-transfected cells, compared with empty vector-transfected controls. β-actin is used as a loading control. (B) Knockdown of HOXD10 expression by siRNA in D19 and B22 increases proliferation as assessed using MTS assay over 96 h. This is partially rescued by the expression of AMOT in these cells. (C) Knockdown of HOXD10 expression in D19 and B22 reduces migration in the Transwell assay, and this is fully rescued by the overexpression of AMOT, to levels higher than controls. (D) Expression of AMOT as assessed using IHC in normal (1 and 2) and HNSCC tissues (3 and 4), demonstrating high expression in primary HNSCC. Photomicrograph overall magnification × 200. *P<0.05, **P<0.01, ***P<0.001, each assay was conducted in triplicate and repeated three times. Data show the mean of triplicate repeats±s.e.m.
