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. 2021 Dec 30;2021:9227897. doi: 10.1155/2021/9227897

Figure 6.

Figure 6

The ARHGEF26-AS1 lncRNA promoted ferroptosis, inhibited cell growth and upregulated the expression of ADAM23 by sponging miR-372-3p in esophageal carcinoma cells. (a) The binding of miR-372-3p to ARHGEF26-AS1, predicted with RNAhybrid 2.12. (b) Regulation of miR-372-3p by ARHGEF26-AS1, assessed through luciferase reporter assays. ∗p < 0.05 vs. miR-NC.; (c) the relative mRNA levels of ADAM23, GPX4, SLC3A2, and SLC7A11 in TE-1 cells cotransfected with the miR-372-3p mimic or shADAM23-1, following the overexpression of ARHGEF26-AS1. Data is presented as the mean ± SD. ∗p < 0.05; (d) the effect of the miR-372-3p mimic and shADAM23-1 on cell proliferation after the overexpression of ARHGEF26-AS1, assessed through the CCK-8 assay. ∗p < 0.05; (e, f) the effect of ARHGEF26-AS1 overexpression on (e) cell proliferation and (f) cell death after treatment with either the miR-372-3p mimic or shADAM23-1. ∗p < 0.05; (g) verification of ARHGEF26-AS1 overexpression through Western blotting following the overexpression of miR-372-3p and the effect of shADAM23-1 on the expression of ADAM23; ∗p < 0.05; (h) proliferation and migration of TE-1 cells, assessed through the wound healing assay; (i) effect of the ARHGEF26-AS1/miR-372-3p/ADAM23 pathway on ferroptosis. ∗p < 0.05.