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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: ALKBH5 enhances lipid metabolism reprogramming by increasing stability of FABP5 to promote pancreatic neuroendocrine neoplasms progression in an m6A-IGF2BP2-dependent manner

Fig. 5

ALKBH5 stabilizes FABP5 mRNA in an m6A-dependent manner. A The expression of m6A in QGP-1 cells with ALKBH5 knockdown was detected by immunofluorescent imaging. B, C The global m6A levels in ALKBH5 knockdown and overexpression cell lines. D The relative expression of FABP5 mRNA in QGP-1 cells treated with DAA. E RIP-qRT-PCR revealing binding enrichment of m6A to FABP5 mRNA in QGP-1 cells with or without ALKBH5 knockdown. F The relative FABP5 mRNA expression in cells with IGF2BP2 knockdown. G The protein expression of FABP5 in QGP-1 cells with IGF2BP2 knockdown was verified by western blots. H RIP-qRT-PCR revealing binding enrichment of IGF2BP2 to FABP5 in QGP-1 cells. I Individual GSEA plots of regulation of mRNA metabolic process and regulation of mRNA stability pathway in RNA-seq data from QGP-1 cells with ALKBH5 knockdown. J FABP5 mRNA half-life (t1/2) was tested at the indicated time points by qRT-PCR in QGP-1 cells with ALKBH5 knockdown. K The knockdown rate of IGF2BP2 was verified by western blots. IG2BP2 inhibition inhibits the growth and motility of pNENs. The CCK-8 (L), colony formation (M, N), and EdU (O, P) assays were applied to evaluate the proliferation ability of QGP-1 cells with the knockdown of IGF2BP2. Q, R Transwell assays of QGP-1 cells with IGF2BP2 knockdown were applied to measure their migration and invasion abilities, magnification: × 100. *p < 0.01, **p < 0.01, ***p < 0.001

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