Cathepsin K modulates invasion, migration and adhesion of oral squamous cell carcinomas in vitro. (9th March 2017)

• Record Type: Journal Article
• Authors: Yamashita, K; Iwatake, M; Okamoto, K; Yamada, S‐i; Umeda, M; Tsukuba, T
• Is Part Of: Oral diseases. Volume 23:Number 4(2017)
• Page Start: 518
• Page End: 525
• Publication Date: 2017-03-09
• Subjects: cathepsin K -- oral squamous cell carcinoma -- invasion; Mouth -- Diseases -- Research -- Periodicals; 617.522
• DOI: 10.1111/odi.12643
• Languages: English
• ISSNs: 1354-523X

Abstract

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. This 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 were expressed in carcinomas. Cathepsin K was predominantly localised 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 β 1 . 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.