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. Author manuscript; available in PMC: 2013 Dec 15.
Published in final edited form as: Int J Cancer. 2012 Jun 28;131(12):2774–2784. doi: 10.1002/ijc.27580

Figure 3. IFNα causes enhancement of HAS2 and VEGF through STAT3 activation in the absence of STAT1.

Figure 3

Figure 3

(a) 1 × 105 of transfected cells were subcutaneously injected to Balb/c nude mice. Other procedures are the same as Fig. 3b. (b) Expression levels of hyaluronic acid synthase (HAS) 2, CD44, and IRF-1 as detected by real-time RT-PCR analysis. PLC/PRF/5 cells were transfected with control siRNA or siRNA for STAT1 and stimulated on the next day with 5.0 × 103 IU/ml of IFNα for 3 hours or left untreated. (c) Hyaluronic acid levels of each tumor as detected by ELISA assay. (d) Activation/expression of STAT1 and STAT3 as detected by western blot analysis. PLC/PRF/5 cells were transfected with control siRNA or siRNA for STAT1 and stimulated on the next day with various concentration of IFNα for 15, 60, or 120minutes. (e) (f) STAT1-knockdown cells were pretreated with or without 100 μM of S31-201, a specific STAT3 inhibitor, before CoCl2 and/or 5.0 × 103 IU/ml of IFNα. (e) Expression levels of HIF-1α as detected by western blot analysis. (f) (g) Expression levels of VEGF as detected by real-time RT-PCR analysis. (g) Control and STAT1-knockdown cells were treated with CoCl2 and/or 100 ng/ml of IL-6. Asterisks indicate significant differences (*1, P<.001, *2, P<.01).