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

Figure 5.

Figure 5

Upregulation of ADAM23 enhanced ferroptosis and inhibited cell growth in esophageal carcinoma cells through the downregulation of miR-372-3p. (a) The binding of miR-372-3p on ADAM23 as predicted by RNAhybrid 2.12. (b) Regulation of ADAM23 by miR-372-3p, assessed through luciferase reporter assays. ∗p < 0.05 vs. miR-NC. (c) The effect of up- and downregulation of miR-372-3p on the expression level of ADAM23, assessed through the WB assay; ∗p < 0.05; (d) real-time PCR results showing the mRNA expression levels of GPX4, SLC3A2, and SLC7A11 in TE-1 cells cotransfected with the miR-372-3p mimic or miR-372-3p inhibitor after the overexpression of ADAM23; ∗p < 0.05; (e) the effect of the miR-372-3p mimic and miR-372-3p inhibitor on cell proliferation after the overexpression of ADAM23, assessed through the CCK-8 assay. ∗p < 0.05; (g) the effect of the miR-372-3p mimic and miR-372-3p inhibitor on (f) cell proliferation and (g) cell death after the overexpression of ADAM23; ∗p < 0.05; (h) the proliferation and migration of TE-1 cells assessed through the wound healing assay. ∗p < 0.05.