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©The Author(s) 2025.
World J Gastroenterol. Apr 28, 2025; 31(16): 104305
Published online Apr 28, 2025. doi: 10.3748/wjg.v31.i16.104305
Published online Apr 28, 2025. doi: 10.3748/wjg.v31.i16.104305
Figure 5 SLC7A11 overexpression reverses the effects of radioresistant cells knockdown lncRNA FTX in sensitivity of ferroptosis and radiotherapy.
A: Downregulation of SLC7A11 promoted radio-sensitivity in HT29R and HCT116R cells; B: Downregulation of SLC7A11 reduced glutathione (GSH) content in HT29R and HCT116R cells; C: CCK-8 assay revealed that SLC7A11 overexpression increased the tolerance of HT29R-shFTX and HCT116R-shFTX cells to ionizing radiation; D: Colony formation assay confirmed the promoting effect of overexpression of SLC7A11 on the growth of HT29R-shFTX and HCT116R-shFTXcells; E: Western blotting analyses determined the expression of ferroptosis-related proteins in HT29R-shFTX and HCT116R-shFTX cells after SLC7A11 over expression; F: Reversal effect GSH content in HT29R-shFTX, HCT116R-shFTX cells after overexpression of SLC7A11; G: Immunofluorescence analyses revealed overexpression of SLC7A11 and upregulated ROS levels in HT29R-shFTX and HCT116R-shFTX cells. aP < 0.05 and bP < 0.01. NC: Negative control.
- Citation: Dai Q, Qu TY, Yang JL, Leng J, Fang L, Zhu QQ, Wu KB, Wu J, Ma JJ, Yu HF. LncRNA FTX promotes colorectal cancer radioresistance through disturbing redox balance and inhibiting ferroptosis via miR-625-5p/SCL7A11 axis. World J Gastroenterol 2025; 31(16): 104305
- URL: https://www.wjgnet.com/1007-9327/full/v31/i16/104305.htm
- DOI: https://dx.doi.org/10.3748/wjg.v31.i16.104305