Fig. 4: Knockdown of SETD2 increases erastin-induced ferroptosis sensitivity mainly through the H3K36me3/FECH pathway in ccRCC. | Cell Death & Disease

Fig. 4: Knockdown of SETD2 increases erastin-induced ferroptosis sensitivity mainly through the H3K36me3/FECH pathway in ccRCC.

From: Knockdown of SETD2 promotes erastin-induced ferroptosis in ccRCC

Fig. 4

A, B qRT-PCR and western blot to analyze the change of FECH and H3K36me3 caused by shSETD2. C Western blot to analyze the change of FECH caused by SETD2 overexpression. D ChIP-PCR analysis of the binding of H3K36me3 to the promoter of FECH in ACHN and OS-RC-2 cell lines. E, F qRT‒PCR and western blot examined the efficiency of FECH overexpression transfected with plasmids. G CCK-8 assays were used to analyse the effect in the shCtrl, shSETD2, erastin, shS+E as well as shS+E + FECH-OE groups on cell viability in ACHN and the effect in the Ctrl, erastin as well as erastin+FECH-OE groups on cell viability in A498. H, I Flow cytometry was used to detect lipid peroxidation in the shCtrl, shSETD2, erastin, shS+E as well as shS+E + FECH-OE groups in ACHN and in the Ctrl, erastin as well as erastin+FECH-OE groups in A498. J, K Levels of MDA and Fe2+ were analyzed in the shCtrl, shSETD2, erastin, shS+E as well as shS+E + FECH-OE groups in ACHN and in the Ctrl, erastin as well as erastin+FECH-OE groups in A498. *P < 0.05, **P < 0.01, ***P < 0.001.

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