作者: Muy-Teck Teh , E. Ken Parkinson , Johanna K. Thurlow , Feng Liu , Farida Fortune
DOI: 10.1111/J.1600-0714.2010.00951.X
关键词:
摘要: J Oral Pathol Med (2011) 40: 67–76 Desmosomes, the intercellular junctions that confer strong adhesion between epithelial cells, are frequently altered in malignancy. However, a comprehensive analysis of these structures has not been carried out oral neoplasia. squamous cell carcinomas (SCCs) and pre-malignant dysplasia can be sub-classified according to their vitro replicative lifespan, where immortal (ID) carcinoma (IC) subsets have p16ink4a p53 dysfunction, telomerase deregulation genetic instability mortal subset (MD MC) do not. We found desmosomal proteins exhibit distinct expression pattern mucosa when compared with epidermis vivo. Microarray data from large panel lines revealed transcript levels DSG3, DSC2/3, DP, PG PKP1 were reduced ID IC. Interestingly, DSG2 was up-regulated MC. Reduction DSG3 up-regulation two independent microarray datasets. Significantly, we demonstrated reduction reversible by using RNAi-mediated knockdown IC cells. The remaining largely disrupted or internalized associated retraction keratin intermediate filaments SCC lines. These findings suggest dysfunction loss components common events class may precede overt