Fig 1: Phosphorylated but not non-phosphorylated hnRNP A0 stabilized the mRNAs of NUDT12, OPN3, and RAB3GAP1.To clarify the mRNAs regulated by hnRNP A0 in non-tumorous cells, a comprehensive analysis of RNA immunoprecipitation and a transcriptome analysis were performed in CoEpiC cells. The combination of immunoprecipitation and a transcriptome analysis identified 36 mRNAs that were directly bound to hnRNP A0 and were stabilized by the hnRNP A0 in CoEpiC cells a (n = 3). Western blotting revealed that the accumulation of phosphorylated hnRNP A0 in the biopsy specimens of colorectal cancer patients was greater than that observed in normal epithelial cells b. The docking simulation indicated that the interaction energy of phospho-hnRNP A0 and mRNAs was decreased compared with non-phospho-hnRNP A0 c. RT-PCR showed that the expression of mRNAs of NUDT12 (HCT116, Panc-1, and MKN45 cells), OPN3 (HCT116 cells), and RAB3GAP1 (HCT116, Panc-1, SUIT-2, and MKN45 cells) was decreased d (n = 3), and RNA-immunoprecipitation revealed that the binding of hnRNP A0 and these mRNAs was weakened in HCT116 cells by treatment with PF-3644022 (an MK2 inhibitor) e (n = 3). RT-PCR showed that the expression of these mRNAs was decreased by gene editing of the hnRNP A0 phosphorylation site (Ser84) f (n = 5). The growth of HCT116 cells was decreased by gene editing of the hnRNP A0 phosphorylation site (Ser 84) g (n = 5). The expression of NUDT12, OPN3, and RAB3GAP1 was increased by the overexpression of hnRNP A0 in hnRNP A0 knockout HCT116 cells h (n = 3). Tumor growth was decreased by PF-3644022 treatment in xenografts of HCT116 cells i (n = 5). The error bars show the S.D. *p < 0.05 by Student’s t-test and an ANOVA.