LncRNA FTX promotes colorectal cancer radioresistance through disturbing redox balance and inhibiting ferroptosis via miR-625-5p/SCL7A11 axis

Figure 3 LncRNA FTX sequester miR-625-5p to regulate intracellular redox and radiosensitivity of colorectal cancer cells. A: The potential binding site between lncRNA FTX and miR-625-5p predicted by Starbase; B: Expression of miR-625-5p in colon and rectal cancer was higher than that in paracancerous tissues; C: Pearson's correlation analysis was performed to determine the correlation between lncRNA FTX and miR-625-5p expression; D: Relative expression of miR-625-5p in HT29R and HCT116R cells; E: Relative expression of miR-625-5p in HT29R-shFTX and HCT116R-shFTX cell lines; F: The targeting relationship between lncRNA FTX and miR-625-5p was confirmed by dual-luciferase reporter assay; G: Transfection of miR-625-5p inhibitor reversed the inhibitory effect of FTX depletion on HT29R and HCT116R cells; H: Colony formation assay confirmed that miR-625-5p inhibitor reversed the survival effect of FTX depletion on HT29R and HCT116R cells; I: MiR-625-5p inhibitor reversed the glutathione content in HT29R and HCT116R cells caused by deletion of FTX; J: Immunofluorescence analyses suggested that miR-625-5p inhibitor altered ROS levels in HT29R-shFTX and HCT116R-shFTX cells. ^aP < 0.05 and ^bP < 0.01. NC: Negative control.