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. 2020 Oct 29;8(2):e001588. doi: 10.1136/jitc-2020-001588

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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TGF-β1 induces CXCL12 production by suppressing miR-200a. (A) TGFβ1 promoted CXCL12 expression in a time-dependent manner. (B) SB431542 blocked the induction effect of TGFβ1 on CXCL12 expression. (C, D) Various concentrations of miR-200a mimics partly neutralized the stimulatory effect of TGFβ1 on CXCL12 expression and ultimately reduced migration of Treg cells in a dose-dependent manner. (E) NPC patients with high TGFβ1 or high p-SMAD3 expression had higher CXCL12 expression compared with those in patients with low TGFβ1 or low p-SMAD3 expression. (F) Kaplan-Meier analysis of recurrence risk and overall survival for concurrent p-SMAD3/CXCL12 expression groups in NPC patients. EBV, Epstein-Barr virus; NPC, nasopharyngeal carcinoma; TGF-β1, transforming growth factor-β1; Treg, regulatory T.