Research Paper Volume 12, Issue 11 pp 10896—10911

SPTBN1 suppresses the progression of epithelial ovarian cancer via SOCS3-mediated blockade of the JAK/STAT3 signaling pathway

Figure 6. SOCS3 overexpression or the JAK2 inhibitor reverses the inhibitory effects of SPTBN1 on cell viability and migration. (A, B) In vitro cell migration assay. * P < 0.05 vs LV-RFP+LV-GFP, #P < 0.05 vs LV-SPTBN1sh+LV-GFP, n=3. (C, D) Comparison of protein (C) and mRNA (D) levels of the EMT-related proteins E-cadherin (E-cad) and Vimentin (Vim). The expression of SOCS3 and E-cadherin was decreased and Vimentin was increased by the loss of SPTBN1, while SOCS3 overexpression reversed the effects of the loss of SPTBN1. *P<0.05 **P<0.01 vs LV-RFP+LV-GFP, ##P<0.01 vs LV-SPTBN1sh+LV-GFP, n=3. (EH) Cell viability was determined by CCK8 assay. SOCS3 overexpression reversed the enhanced cell viability due to the loss of SPTBN1 in A2780 (E) and HO8910 cells (F). #P<0.05, ##P<0.01 vs LV-RFP+LV-GFP, *P<0.05 vs LV-SPTBN1sh+LV-GFP, n=3. The JAK2 inhibitor Ag490 or tofacitinib (Tofa) inhibited cell viability and reversed the promoting effect of the loss of SPTBN1 in A2780 (G) and HO8910 cells (H). *P<0.05, **P<0.01 vs LV-RFP, #P<0.05 vs LV-SPTBN1sh, n = 3.