Fig. 4From: Aberrant overexpression of transcription factor Forkhead box D1 predicts poor prognosis and promotes cancer progression in HNSCCFOXD1 knockdown inhibits cell migration and invasioncell proliferation, cell migration and invasion and triggers apoptosis in HNSCC cells. A: Endogenous FOXD1 protein expression was measured in a panel of HNSCC cell lines as compared to normal human oral keratinocytes (HOK). B: Endogenous FOXD1 was efficiently silenced by two siRNAs (siFOXD1–1, siFOXD1–2) in FADU and Cal27 cells. Non-targeting siRNA was utilized as negative control (siNC). C: Cell proliferation was remarkably suppressed when endogenous FOXD1 was silenced as measured by CCK8 assays. D, E: Increased percentages of cell undergoing apoptosis were evident following FOXD1 knockdown as assayed by Annexin V-PI staining. F, G: Cell migration was determined in cells with FOXD1 knockdown by wound-healing assay in Cal27 cells. H-G: Cell invasion was determined in cells with FOXD1 knockdown by transwell invasion assay in Cal27 and Fdau cells. K-M: The protein and mRNA abundance of migration/invasion-relevant marker E-cadherin, N-cadherin, snail and Vimentin was compared in cells infected siFOXD1 or control siNC. Scale bar: 100 μm. Data shown from three independent experiments, *P < .05, **P < .01, Kruskall-Wallis testBack to article page