BACKGROUND: Kallikrein-related peptidases (KLKs) are a family of serine 
proteases that have been shown to be dysregulated in several malignancies 
including ovarian cancer. The control of kallikrein genes and their 
physiological function in cancer is not well understood. We hypothesized that 
microRNAs (miRNAs) represent a novel mechanism for post-transcriptional control 
of KLK expression in cancer.
METHODS: We first analysed miRNA expression in ovarian cancer in silico. A total 
of 98 miRNAs were reported to have altered expression in ovarian cancer. Three 
of these miRNAs were predicted to target KLK10. We experimentally verified the 
predicted miR-KLK10 interaction using two independent techniques, a luciferase 
assay with a construct containing the KLK10 3' untranslated region (UTR), 
pMIR-KLK10, and measuring KLK10 protein levels after transfection with miRNA.
RESULTS: When we co-transfected cells with pMIR-KLK10 and either let-7f, 
miR-224, or mR-516a, we saw decreased luciferase signal, suggesting that these 
miRNAs can target KLK10. We then examined the effect of these three miRNAs on 
KLK10 protein expression and cell growth. Transfection of all miRNAs, let-7f, 
miR-224, and miR-516a led to a decrease in protein expression and cellular 
growth. This effect was shown to be dose dependent. The KLK10 protein levels 
were partially restored by co-transfecting let-7f and its inhibitor. In 
addition, there was a slight decrease in KLK10 mRNA expression after 
transfection with let-7f.
CONCLUSION: Our results confirm that KLKs can be targeted by more than one 
miRNA. Increased expression of certain miRNAs in ovarian cancer can lead to 
decreased KLK protein expression and subsequently have a negative effect on cell 
proliferation. This dose-dependent effect suggests that a 'tweaking' or 
'fine-tuning' mechanism exists in which the expression of one KLK can be 
controlled by multiple miRNAs. These data together suggest that miRNA may be 
used as potential therapeutic options and further studies are required.