Fig. 5
From: LncRNA FTX promotes myocardial fibrosis by sponging miR-335-3p to regulate TFEC/ILK signaling
Lnc FTX acts as a ceRNA to sponge miR-335-3p. (A) Multiple LncRNAs were predicted to have binding sites with miR-335-3p, and the expression levels of these LncRNAs were assessed in TGF-β1-treated CFs. Lnc FTX was most upregulated in TGF-β1-treated CFs. (B–D) CFs were transfected with plasmids to silence Lnc FTX, XIST, or Lnc LINC00294, and the miR-335-3p levels were examined. Only silencing Lnc FTX affected the level of miR-335-3p. (E) FISH assay was conducted to confirm the subcellular localization of Lnc FTX in CFs. (F) Subcellular fractionation followed by qRT-PCR was performed to verify the location of Lnc FTX. (G,H) RIP assay assessed the interaction between Lnc FTX and miR-335-3p. (I) The predicted binding sequence between Lnc FTX and miR-335-3p. (J,K) Luciferase reporter assays validated the binding relationship between Lnc FTX and miR-335-3p in both 293T cells and CFs. All these results indicate that Lnc FTX functioned as a ceRNA and sponged miR-335-3p. **p < 0.01 vs. indicated groups. ceRNA, competing endogenous RNA; CFs, cardiac fibroblasts; FISH, fluorescence in situ hybridization.
