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models demonstrate that genetic depletion of KIAA1429 markedly inhibits tumor growth, as well as cancer cell proliferation, migration, and invasion. Mechanistically, KIAA1429 directly binds to the 3' untranslated region (3' UTR) of MYC mRNA and catalyzes site-specific m6A methylation, thereby enhancing transcript stability and augmenting MYC protein expression. Collectively, these findings identify KIAA1429 as a critical m6A-dependent post-transcriptional regulator of MYC and nominate the KIAA1429-MYC regulatory axis as a promising therapeutic target in ccRCC.
Zhu et al. (Tue,) studied this question.