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Fig. 4 | BMC Cancer

Fig. 4

From: Aberrant overexpression of transcription factor Forkhead box D1 predicts poor prognosis and promotes cancer progression in HNSCC

Fig. 4

FOXD1 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 test

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