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. 2018 Nov 9;41(2):753–764. doi: 10.3892/or.2018.6859

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Copyright: © Hou et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 5. — TROP2 mediates oncogenic effects by promoting the activation of the JAK2/STAT3 pathway. (A) Relative mRNA expression of STAT3 target genes in TROP2-knockdown or control U-87 MG cells and LN-229 cells. Transcript levels were normalized to GAPDH. (B and C) Western blot analysis of JAK2^Tyr1007/1008, total JAK2, STAT3^Tyr705, total STAT3, CCND1, survivin, MMP2 and VEGF levels in TROP2-silenced U-87 MG and LN-229 cells and xenograft tumors, GAPDH was used as loading control. (D) Representative IHC staining for TROP2, p-JAK2, and p-STAT3 in GBM samples from patients. All data are shown as the means ± SD; **P<0.01, ***P<0.001. All P-values are based on control vs. treatment group. TROP2, trophoblast cell surface antigen 2; GBM, glioblastoma.