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. 2015 Jan 1;25(1):85–94. doi: 10.1089/thy.2014.0155

FIG. 5.

FIG. 5.

Ectopic overexpression of transmembrane protease serine 4 (TMPRSS4) promotes the cyclic adenosine monophosphate response element-binding protein (CREB)-induced cyclin D1 transcription. (A) Cellular mRNA levels of cyclin D1 were elevated in TMPRSS4-overexpressing thyroid cancer cells. TMPRSS4-induced cyclin D1 expression could be reversed by CREB knockdown. (B) Ectopic expression of TMPRSS4 in the studied cells promoted the phosphorylation of CREB (Ser133). α-tubulin served as the sample loading control. (C) Indicated cells were transduced with the CREB firefly luciferase reporter plasmid, using cotransfected pRL-TK to normalize the luciferase values. Data are presented as fold induction relative to vector-control cells. (D) Knockdown of CREB in TMPRSS4-overexpressing thyroid cancer cell lines was analyzed by Western blotting. α-Tubulin was used as a loading control. (E) TMPRSS4-induced cell growth could be reversed by CREB knockdown. For (A), (C), and (E), results derived from three independent experiments are expressed as mean±standard deviation. *p<0.05.