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Fig. 9. Effects of overexpression of PKC and STAT3 on keratinocytes proliferation and cell death. Keratinocytes were infected for 1 hour with (A) recombinant adenoviruses ß-Gal, PKC, WT STAT3, DN STAT3 or double infected with DN PKC followed by WT STAT3 or with DN STAT3 followed by WT PKC infection. (B) with recombinant adenoviruses ß-Gal, PKC, DN PKC, WT STAT3, DN STAT3 and STAT3 serine mutant (SmS) and un-treated (–) or treated (+) with insulin. Twenty-four hours following infection, cell proliferation was analyzed by [³H]thymidine incorporation as described in Materials and Methods. Results are presented as cpm/µg protein. Each bar represents the mean of three determinations in a plate from the same culture. Experiments were repeated at least three times. (mean ± s.d.). Significant differences were observed between ß-gal control values and those for WT STAT3 (P<0.001) and PKC (P<0.0005). (C) Keratinocytes were infected with recombinant adenoviruses encoding ß-Gal, PKC, WT STAT3, DN STAT3 and STAT3 serine mutant (SmS). Following infection (24 hours) FACS cell-cycle analysis of propidium-iodide-stained keratinocytes was performed. Apoptotic cell death was defined as the sub-G1 population (Apo, percentage of sub-G1 population) and proliferation was identified as the population of S-phase cells (S, percentage of S-phase population).

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