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. 2019 Jan 22;8:682. doi: 10.3389/fonc.2018.00682

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Copyright © 2019 Zheng, Cai, Chen, Chen, Zhu, Zhong and Xie.

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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CXCL13/CXCR5 axis promoted ccRCC progression partly through PI3K/AKT/mTOR pathway. (A) GSEA was performed to identify associated pathways between CXCL13⁺CXCR5⁺ and CXCL13⁻CXCR5⁻ ccRCC tissues. PI3K/AKT/mTOR pathway, JAK/STAT3 pathway, TNF-α/NF-kB pathway, KRAS pathway, and P53 pathway were activated in CXCL13⁺CXCR5⁺ ccRCC tissues. (B) Western blotting analysis of these associated pathway in ccRCC cells. The expression of PI3K, p-AKT, and mTOR in ccRCC cells (Caki-2 and ACHN) were upregulated when incubated with CXCL13, and downregulated with CXCR5 knockdown. (C) Relative expression of associated pathway protein in ccRCC cells. GAPDH was used as normal control (Student's t-test, *P < 0.05).