Kallikrein-Related Peptidase mRNA Expression in Adenoid Cystic Carcinoma of Salivary Glands: A Polymerase Chain Reaction Study.

Kallikrein-related peptidases (KLKs) are a group of 15 serine proteases implicated in a variety of biological processes. Aberrant expression of KLKs has been associated with the development of certain cancers. However, the role of KLKs in salivary tumors has not been extensively studied. This study evaluated the expression of KLKs in both adenoid cystic carcinoma (ACC) and normal salivary gland tissue. We isolated total RNA from 39 formalin-fixed, paraffin-embedded samples, which included 24 ACCs and 15 normal salivary gland tissues. Complementary DNA, synthesized by reverse transcription, was combined with gene specific kallikrein primers (KLK1-KLK15) to allow for quantitative real-time PCR. Data was normalized to a ß-actin housekeeping gene. Relative quantification analysis was performed using the ΔCq method. KLK1-KLK15 expression was observed in both tissue types. However, KLK1, KLK8, KLK11, and KLK14 were found to be downregulated in ACC. We propose that this may represent a multi-parametric panel providing diagnostic and prognostic information.

Kallikrein-related peptidase expression in odontogenic cysts and tumors: An immunohistochemical comparative study.

AIM: The aim of the present study was to profile the expression of human kallikrein (KLK)-related peptidases (KLK) in odontogenic lesions. METHODS: Paraffin-embedded, formalin-fixed, non-odontogenic (control) and odontogenic lesions were stained for KLK using a standard immunohistochemical technique. The intensity and proportion of epithelial cells stained was scored. Reverse transcription-polymerase chain reaction was utilized to evaluate KLK 1-15 mRNA expression in ameloblastomas. RESULTS: KLK 3, 4, 9, 11, and 14 were present in all lesions. KLK 3 staining was increased in ameloblastomas and keratocystic odontogenic tumors. KLK 5 was present only in Keratocystic odontogenic tumor. KLK 6 was significantly higher in ameloblastomas than in other lesions. For KLK 7, keratocystic odontogenic tumors and nasopalatine duct cysts were significantly different. KLK 6, 8, 10, 11, and 13 were significantly higher in ameloblastomas than in other lesions. KLK 9 was increased in keratocystic odontogenic tumors and dentigerous cysts. The expression of KLK 1, 4, 7, 8, 10, and 12 mRNA was found in ameloblastomas. CONCLUSION: The results suggested that KLK 6, 8, 10, and 13 could be involved in the progression of ameloblastomas. KLK 10 could have a greater role in odontogenic lesions, rather than non-odontogenic lesions. Future studies aim to define the specific roles of KLK cascades in odontogenic lesions.