Fig. 5: MeRIP-seq and RNA-seq combined with multi-omics analysis identified SNTB1 as the downstream target of ZC3H13.

A Top sequence motif identified from MeRIP-seq peaks in control and ZC3H13-depleted cells. B Distribution of reduced m6A peaks generated by ZC3H13 inhibition across all the mRNAs. C Intersection of ZC3H13 related differential genes in MeRIP, RNA seq, and multi-omics data. D The top 20 genes with the greatest differences between the control and ZC3H13-depleted groups according to the RNA-seq data. Changes in the mRNA (E) and protein (F) expression levels of downstream target molecules after the knockdown of ZC3H13. Changes in the mRNA (G) and protein (H) expression levels of downstream target molecules after the overexpression of ZC3H13. I The predicted results for SNTB1 mRNA on the SRAMP website indicate potential sites for m6A modification. J, K MeRIP assays detected the m6A modification of SNTB1 by using anti-IgG and anti-m6A antibodies. L RNA obtained after MeRIP was reverse transcribed for RT-qPCR to detect the m6A modification level of SNTB1. M The wild-type or mutant m6A consensus sequence is linked to firefly luciferase. N Effect of ZC3H13 overexpression on the luciferase activity of the wild-type and mutant SNTB1 fusion reporter genes. O Expression of SNTB1 mRNA in control and shZC3H13 AGS cells treated with actinomycin D (5 μg/ml) for different durations. Relationship between the expression of SNTB1 and OS (P), FPS (Q), and PPS (R) in GC tissue. S Representative images showing high or low expression of ZC3H13, SNTB1, E-cadherin, N-cadherin, Vimentin, and β-catenin in 60 gastric tumor samples (magnification, 200×). T Correlations of ZC3H13 expression with SNTB1, E-cadherin, N-cadherin, Vimentin and β-catenin expression in 60 gastric tumor tissues. *P < 0.05, **P < 0.01, and ***P < 0.001 represent varying degrees of significance between the indicated groups.