Fig. 2: LncRNA TGILR was directly induced by the canonical TGFbeta/SMAD3 axis. | Cell Death & Disease

Fig. 2: LncRNA TGILR was directly induced by the canonical TGFbeta/SMAD3 axis.

From: A novel TGFbeta/TGILR axis mediates crosstalk between cancer-associated fibroblasts and tumor cells to drive gastric cancer progression

Fig. 2

a Identification of the TGFbeta-regulated lncRNAs in GES-1 cell line by RNA-seq analysis. The differentially expressed lncRNAs (log2FC > 1, p < 0.05) in GES-1 cells exposed to TGFbeta (10 ng/ml) are shown in the heatmap. b The log2FC and p values per lncRNA were shown in the volcano plot. TGILR was the most significant lncRNA induced by TGFbeta. c TGILR expression can respond to different concentrations of TGFbeta and exhibits a certain concentration dependence in GES-1 cell line. d, e The phenomenon that TGFbeta activates TGILR expression is widely present in different GC cell lines and different tumor cell lines. f The TGFbeta Type I receptor inhibitor LY364947 (5 μM) blocks the induction effect of TGFbeta on TGILR expression in the GES-1 and AGS cell lines. g Overexpression of SMAD3 enhanced the induction effect of TGFbeta on TGILR expression in GES-1 and AGS cell lines. h Chip-seq analysis by the Cistrome database showed that transcription factor SMAD3 directly binds to TGILR promoter. i, j A Chip-PCR assay confirmed that transcription factor SMAD3 directly binds on TGILR promoter in the AGS cell line. ****, P < 0.0001; ***, P < 0.001; **, P < 0.01; *, P < 0.05.

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