Fig. 5: ILF3 modulates SLC3A2 mRNA stability by directly binding to the 3’ UTR. | Cell Death & Disease

Fig. 5: ILF3 modulates SLC3A2 mRNA stability by directly binding to the 3’ UTR.

From: ILF3 promotes colorectal cancer cell resistance to ferroptosis by enhancing cysteine uptake and GSH synthesis via stabilizing SLC3A2 mRNA

Fig. 5

A, B RT-qPCR analysis of SLC7A11 and SLC3A2 mRNA levels in ILF3 knockdown SW620 and DLD-1 cells. C RIP assay evaluating the relative enrichment of SLC7A11 and SLC3A2 mRNA in ILF3-RNA binding complexes; anti-IgG served as a negative control. D RIP assay evaluating the relative enrichment of SLC3A2 mRNA in ILF3 knockdown cells. E mRNA stability analysis of SLC3A2 in ILF3 knockdown cells after ActD (5 μg/mL) treatment. F, G Schematic representation of the SLC3A2 luciferase reporter plasmid and relative luciferase activities in ILF3 knockdown cells, calculated as the ratio of firefly to Renilla luciferase activity. H, I Schematic representation of wild-type and three mutant SLC3A2 3’ UTR luciferase reporter plasmids and relative luciferase activities in ILF3 knockdown cells. J Cell viability in ILF3 knockdown cells with or without SLC3A2 overexpression. K, L GSH levels and cystine uptake in ILF3 knockdown cells with or without SLC3A2 overexpression. M Xenograft mouse model constructed using ILF3 knockdown cells with or without SLC3A2 overexpression. Tumor volume was measured every 3 days. N Tumor weight. O Immunohistochemical staining of SLC3A2 and Ki-67. Scale bar = 20 μm.

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