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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.

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TGFβ1 suppresses miR-200a by enhancing the formation of the SMAD3/c-JUN complex. (A) (B) WB and qRT-PCR detection verified that c-JUN is a downstream factor of the TGFβ1-SMAD3 axis; TGF-β1 suppressed miR-200a by activating the SMAD3-c-JUN pathway. (C) Quadruple-color confocal microscopy colocalization of TGFβ1, SMAD3 and c-JUN. (D) Coimmunoprecipitation (Co-IP) analysis indicated that SMAD3 and c-JUN can form a complex to mediate TGFβ1-induced transcription and that EBNA1 determines the SMAD3/c-JUN interaction in a TGF-β1-dependent manner. (E) NPC patients with high TGFβ1 or high p-SMAD3 expression had higher c-JUN and p-c-JUN expression compared to 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/p-c-JUN expression groups in 105 NPC patients. ANOVA, analysis of variance; NPC, nasopharyngeal carcinoma; TGF-β1, transforming growth factor-β1; WB, western blot.