Fig. 7
From: LncRNA FTX promotes myocardial fibrosis by sponging miR-335-3p to regulate TFEC/ILK signaling
Lnc FTX regulates TFEC via sponging miR-335-3p. (A,B) CFs were transfected with a Lnc FTX overexpression vector (Lnc FTX-OE) or Lnc FTX knockdown plasmid (sh-Lnc FTX), along with their respective negative controls (NC-OE and NC-sh). TFEC protein expression was analyzed by western blotting and quantified. (C) ILK mRNA levels were measured using qRT-PCR. Lnc FTX overexpression significantly increased TFEC expression, whereas Lnc FTX knockdown reduced TFEC levels. (D,E) RIP assays were performed to examine the enrichment of TFEC and miR-335-3p. TFEC and miR-335-3p were enriched in the Ago2 group. (F,G) Biotin-coupled miR-335-3p pull-down assays assessed the enrichment of Lnc FTX and TFEC. The Biotin-miR-335-3p group showed significantly higher enrichment of Lnc FTX and TFEC. (H,I) CFs were transfected with miR-335-3p mimic alone or co-transfected with miR-335-3p mimic and Lnc FTX overexpression vector, and TFEC protein expression was analyzed by western blotting and quantified. Overexpression of miR-335-3p significantly reduced TFEC protein expression, and this effect was partially reversed by overexpression of Lnc FTX. *p < 0.05 and **p < 0.01 vs. indicated groups. CFs, cardiac fibroblasts; NC-OE: overexpression negative control (empty vector); NC-sh: short hairpin RNA negative control; sh-Lnc FTX: short hairpin RNA against Lnc FTX; Lnc FTX-OE: Lnc FTX-overexpressing vector.
