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Figure 2 | Reproductive Biology and Endocrinology

Figure 2

From: Oncostatin M stimulates cell migration and proliferation by down-regulating E-cadherin in HTR8/SVneo cell line through STAT3 activation

Figure 2

Effects of OSM, STAT3 inhibitor, and STAT3 siRNA on protein expression of STAT3, phosphorylated STAT3 and E-cadherin. STAT3 phosphorylation in HTR8/SVneo cells was transiently stimulated with OSM (A). The effect of OSM on STAT3 phosphorylation was checked by pretreatment with stattic (1 μM for 1 h) compared to the OSM treatment, *p < 0.05 (B). Cells were pretreated with the STAT3 inhibitor stattic (0.5 and 1 μM) for 1 h prior to treatment with or without OSM (20 ng/mL). Protein expression of E-cadherin was analyzed by western blotting (C). The expression was quantified, and the values shown are means ± SEM (D) compared to the control, *p < 0.05. Western blots of STAT3, phosphorylated STAT3, and E-cadherin analyzed 24 h after transfection (E). STAT3 and phosphorylated STAT3 protein expressions were reduced significantly after siRNA transfection compared with non-transfected control cells (p < 0.05, p < 0.05, 63.6% and 74.3%, respectively), whereas transfection with a non-targeted siRNA had no effect on STAT3 protein expression levels. Western blots of E-cadherin protein show significantly restored E-cadherin expressions (p < 0.05, 75.6%), compared to the OSM-induced E-cadherin suppression without affecting GAPDH protein expression. Non-targeted negative control siRNA did not affect OSM-induced E-cadherin suppression. The results are representative of 3 independent experiments.

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