Fig. 5

circKIAA1797 inhibits cuproptosis by suppressing FDX1 and LIPT1 expression. (A) KEGG pathway enrichment analysis of proteins downstream of circKIAA1797. (B) ICP‒MS detection of copper in cells after the stable silencing of circKIAA1797. (C) Reduced glutathione (GSH) levels in cells were detected after the transient silencing and overexpression of circKIAA1797. (D and E) Detection of the direct binding of circKIAA1797 to the FDX1 mRNA by ChIRP-qPCR and agarose gel electrophoresis. (F) Changes in FDX1 mRNA levels detected by qPCR after the transient silencing and overexpression of circKIAA1797. (G) Changes in FDX1 protein levels detected by Western blot after the transient silencing and overexpression of circKIAA1797. (H and I) Detection of circKIAA1797 binding to STAT1 by RIP-qPCR and agarose gel electrophoresis. (J) CLIP-qPCR results showing that circKIAA1797 binds to STAT1. (K) Western blot analysis of STAT1 protein expression after the transient silencing or overexpression of circKIAA1797. (L) The JASPAR website was used to predict the ability of the STAT family to bind to the FDX1, DLD, DLAT, LIPT1, and LIAS promoter regions. (M) ChIP‒qPCR results showed STAT1 binding to the DLAT, LIPT1, DLD, and LIAS promoter regions. (N) ChIRP–qPCR results showed the circKIAA1797-mediated regulation of LIPT1 transcription through the STAT1 protein. (O) Western blot analysis of LIPT1 protein expression after the transient silencing or overexpression of circKIAA1797. (P) DLAT oligomerization was detected by IF staining after the transient silencing of STAT1 in A549 and H1299 cells. (Q) DLAT oligomerization was detected by IF staining after the transient silencing and overexpression of circKIAA1797 in A549 and H1299 cells