Analysis of L1 Cell Adhesion Molecule and Fucosyltransferase 8 Expression in Cells After Stretch and Human EACSCC Tissue.

Abstract

Background: External auditory canal (EAC) squamous cell carcinoma (SCC) is classified as a rare cancer and has a poor prognosis at advanced stages. Mechanical stress has been implicated in external auditory canal squamous cell carcinoma (EACSCC), but the molecular mechanism has not been elucidated. Mechanotransduction is well-known for Yes-associated protein (YAP) signaling. When YAP is translocated to the nucleus, the L1 cell adhesion molecule (L1CAM) is activated as an effector of mechanotransduction. Core fucosylation of L1CAM by Fucosyltransferase 8 (FUT8) has been implicated in the degree of tumor malignancy, modulating cleavage of the extracellular domain of L1CAM. Methods: In this study, an expression analysis of YAP, L1CAM, and FUT8 was performed by stretch assay in vitro. Immunohistochemistry was also performed in human EACSCC and normal skin specimens. Results: The labeling index of FUT8-positive cells exhibited YAP nuclear translocation under stretch stress was significantly higher in a human SCC cell line (HSC1) than in a human keratinocyte cell line. Stretch stress significantly increased the expression levels of full-length L1CAM in HSC1 cells. Moreover, colocalization of FUT8 and L1CAM was demonstrated immunohistochemically in advanced human EACSCC tissues. Conclusion: These results suggested that L1CAM expression is increased under mechanotransduction and may possibly avoid L1CAM cleavage by FUT8 modulation.