Fig. 5
CIH-induced ferroptosis is reversed by the overexpression of SLC7A11 in the BEAS-2B cells (n = 5). (A) The transfection efficiency of SLC7A11 was verified through qRT-PCR; (B), The transfection efficiency of SLC7A11 was confirmed through Western Blot; (C), SLC7A11 overexpression reversed the viability of BEAS-2B cells; (D), SLC7A11 overexpression reversed the levels of apoptosis rate; (E), SLC7A11 overexpression reversed the levels of ROS; (F), SLC7A11 overexpression reversed the levels of Fe2+; (G), SLC7A11 overexpression reversed the mRNA levels of GPX4, but did not affect the mRNA levels of HIF-1α; (H), SLC7A11 overexpression reversed the protein levels of GPX4, but did not affect the protein levels of HIF-1α. (I), A binding site exists between the HIF-1α and the promoter region of SLC7A11. ChIP-qPCR results showed that HIF-1α was significantly enriched in the SLC7A11 promoter region at -658–557 bp, 46–165 bp, and 467–662 bp, respectively. SLC7A11-OE compared with Vector: &p < 0.05; &&&p < 0.001; CIH compared with control: **p < 0.01; *** p < 0. 001; ****p < 0.0001; CIH + SLC7A11-OE compared with CIH + Vector: #p < 0.05; ##p < 0.01; ###p < 0.001; ns p > 0.05; IgG IP compared with HIF-1α IP: @@p < 0.01; @@@p < 0.001.
