INTRODUCTIONrnEMT is a biochemical process that enables epithelial cells to exhibit traits of a mesenchymal phenotype.1–3 Cell surface proteins (E-cadherin, N-cadherin, ZO-1 and Integrin family members), cytoskeletal proteins (α-SMA and Vimentin), extracel-lular matrix proteins (collagens, FN1 and Laminin) and some transcription factors (PRRX1, SNAIL1, SLUG, TWIST1/2 and ZEB1/2) are biomarkers of EMT.4–5 Previous immunohistochemical analyses of HNSCC samples showed that FN1 is overexpressed in the tumour stromal region and at the invasive front of the tumour.6 FN1 is upregulated in many tumours and is then referred to as the cellular or'oncofoetal' variant (OncFN). OncFN is a marker of the tumour vasculature7 and a principal component of the metastatic microenvironment, termed the premetastatic niche, in many tumours.8 Multivariate analysis showed that overexpression of OncFN was associated with a trend towards significantly lower overall survival rates.9 Although the role of FN1 in tumours has been explained, the intracellular metabolism of FN1 and its mechanism are not sufficiently understood. As FN1 is an essential mesenchymal phenotypic indicator, its degradation pathway requires further investigation.