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. 2020 Oct 28;10:585292. doi: 10.3389/fonc.2020.585292

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Copyright © 2020 Liao, Chen, Yu, Huang, Hu, Su, He, Zou, Zhang and Lin.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ARL4C regulates β-catenin expression through the JAK2/STAT5A signal pathway. (A–D) The expression of p-JAK2 in HCC827-ARL4C-SH, HCC827-Vector, and HCC827 (control) cells (A) and in HCC827/ER-ARL4C-OE, HCC827/ER-Vector, and HCC827/ER (control) cells (B) detected by Western blot. STAT5 protein expression in HCC827-ARL4C-SH, HCC827-Vector cells (C) and in HCC827/ER-ARL4C-OE, HCC827/ER-Vector cells (D) also detected by Western blot. (E) The enrichment of the β-catenin (CTNNB1) promoter in immunoprecipitated (IP) STAT5 and the input of STAT5 in HCC827/ER-ARL4C-OE, HCC827/ER-Vector, HCC827-ARL4C-SH, and HCC827-Vector and followed by Western blot. Unrelavant IgG was used as a negative control staining. (F,G) Luciferase activity in HEK293T cells (F) and HCC827 cells (G) co-transfected with pGL3-CTNNB1-Luc or mut-pGL3-CTNNB1-Luc and HBLV-ARL4C-SH3 by the Dual-Luciferase Reporter Assay System, ***P < 0.001.