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 5. Loss of SPTBN1 activates the JAK/STAT3 signaling pathway through downregulation of SOCS3. (A) Assessments of JAK/STAT signaling pathway-associated proteins by western blot after SPTBN1 knockdown cooperated with SOCS3 overexpression in HO8910 cells (left), and SPTBN1 overexpression cooperated with SOCS3 knockdown (right). (B) DNA gel electrophoresis after PCR. Mouse embryonic fibroblasts (MEFs) were cultured from SPTBN1-/- embryos (n=2), SPTBN1+/- embryos (n=3) and wild-type embryos (n=2). The genotypes of MEFs were identified by PCR and DNA gel electrophoresis. Lanes 1 and 2: SPTBN1-/- MEFs; lanes 3, 4, and 5: SPTBN1+/- MEFs; lanes 6 and 7: SPTBN1-/- MEFs. (C) Assessments of EMT and JAK/STAT3 signaling pathway-associated proteins by western blot in SPTBN1-/-, SPTBN1+/-, and SPTBN1+/+ MEFs. Lanes 1 and 2: SPTBN1-/- MEFs; lanes 3, 4, and 5: SPTBN1+/- MEFs; lanes 6 and 7: SPTBN1-/- MEFs. Loss of SPTBN1 can promote EMT, inhibit SOCS3 and activate the JAK/STAT signaling pathway.