Cathepsin K modulates invasion, migration, and adhesion of oral squamous cell carcinomas in vitro

Abstract

Objective

Cathepsin K was initially discovered as an osteoclast-specific cysteine proteinase, but the enzyme is also expressed in various cancers including oral squamous cell carcinomas. The present study aimed to clarify the function of cathepsin K in oral squamous cell carcinomas.

Materials and methods

Expression levels of cathepsin K were examined in six types of cell carcinomas. Carcinomas overexpressing cathepsin K were constructed. Effects of cathepsin K overexpression and treatment with odanacatib, a specific cathepsin K inhibitor, on cell invasion, migration, and adhesion were analysed.

Results

Different levels of cathepsin K was expressed in carcinomas. Cathepsin K was predominantly localized in lysosomes. Cathepsin K overexpression impaired the proliferation of carcinomas. Invasion analysis showed that cathepsin K overexpression enhanced invasion and migration of carcinomas, whereas inhibition of cathepsin K by odanacatib caused the opposite effects in carcinomas. Cathepsin K overexpression also increased cell adhesion and slightly increased surface expression of the adhesion receptor CD29/integrin β₁.

Conclusions

The enhanced invasion of carcinomas resulting from cathepsin K overexpression is probably due to the increased cell migration and adhesion. Thus, cathepsin K is implicated not only in protein degradation but also in invasion, migration, and adhesion of oral squamous cell carcinomas.

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