Fig. 7

.circKIAA1797 promotes lung cancer development by inhibiting cuproptosis. (A) After the transient silencing of YBX1, Western blot analysis was performed to detect FDX1 protein expression. (B) After YBX1 was silenced, a CCK-8 assay was performed to detect changes in cellular resistance to cuproptosis. (C) After the transient overexpression of circKIAA1797, Western blot analysis was performed to detect FDX1 protein expression. (D) After the simultaneous overexpression of circKIAA1797 and FDX1, an EdU assay was performed to detect changes in cell proliferation. (E) After the simultaneous overexpression of circKIAA1797 and LIPT1, an EdU assay was performed to detect changes in cell proliferation. (F and G) After the simultaneous overexpression of circKIAA1797 and FDX1, a CCK-8 assay was performed to detect changes in cellular resistance to cuproptosis. (H and I) After the simultaneous overexpression of circKIAA1797 and LIPT1, a CCK-8 assay was conducted to detect changes in cellular resistance to cuproptosis. (J) The presence of o8G on circKIAA1797 and the o8G reader YBX1 increased circKIAA1797 stability and nuclear export. circKIAA1797 can inhibit FDX1 protein expression by decreasing the stability of the FDX1 mRNA and directly binding the transcription factor STAT1, inhibiting LIPT1 transcription, whereas circKIAA1797 promotes mPTP closure, ultimately inhibiting cuproptosis to promote lung cancer development