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In glioblastoma and hepatocarcinoma, the expression level of SLC7A11 can be upregulated in an m 6 A-dependent manner with the assistance of METTL3 and IGF2BP1 via the inhibition of SLC7A11 mRNA degradation and increased SLC7A11 mRNA splicing and maturation [212, 213]
CD38 and regulation of the immune response cells in cancer
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