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We investigated the regulation of STAT3 by SPTBN1 and/or SMAD3 through the collaboration with CRE-binding transcription factors and propose a molecular mechanism responsible for the tumor-suppressive function of SPTBN1 and SMAD3 in the inhibition of STAT3 to prevent HCC development.

Transcriptional regulation of STAT3 by SPTBN1 and SMAD3 in HCC through cAMP-response element-binding proteins ATF3 and CREB2