Non-melanoma skin cancers (NMSC) are the most common malignancies in caucasians 
worldwide. Insulin-like growth factor-binding protein-7 (IGFBP7) was suggested 
to function as a tumor suppressor gene in several cancers, and to play a role in 
the proliferation of keratinocytes. A-to-I RNA editing is a post-transcriptional 
mechanism frequently used to expand and diversify transcriptome and proteome 
repertoire in eukaryotic cells. A-to-I RNA editing can alter codons, substitute 
amino acids and affect protein sequence, structure, and function. Two editing 
sites were identified within the IGFBP7 transcript. To evaluate the expression 
and editing of IGFBP7 mRNA in NMSC compared to normal epidermis. We examined the 
expression and mRNA editing level of IGFBP7 in 22 basal cell carcinoma (BCC), 15 
squamous cell carcinoma (SCC), and 18 normal epidermis samples that were 
surgically removed from patients by the Mohs Micrographic Surgery procedure. We 
studied the effect of IGFBP7 editing on an immortalized HaCaT keratinocyte cell 
model. IGFBP7 mRNA is over expressed in BCC and SCC compared to normal 
epidermis. Moreover, the IGFBP7 transcript is highly edited in normal epidermis, 
but its editing is significantly reduced in BCC and SCC. The edited form of 
IGFBP7 can inhibit proliferation and induce senescence in cultured 
keratinocytes. This study describes for the first time A-to-I editing in the 
coding sequence of a tumor suppressor gene in humans, and suggests that IGFBP7 
editing serves as a fine-tuning mechanism to maintain the equilibrium between 
proliferation and senescence in normal skin.