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Fig. 4 | Biology Direct

Fig. 4

From: N6-methyladenosine-mediated SH3BP5-AS1 upregulation promotes GEM chemoresistance in pancreatic cancer by activating the Wnt signaling pathway

Fig. 4

ALKBH5/IGF2BP1-mediated m6A modification contributed to SH3BP5-AS1 overexpression. A ALKBH5 was downregulated in pancreatic cancer tumor tissues compared with the paired adjacent tissues, as revealed by RT-qPCR. B The negative correlation between the levels of ALKBH5 and SH3BP5-AS1 was confirmed using the TCGA database. C The RIP RT-qPCR assay revealed that m6A modification of SH3BP5-AS1 was mainly enriched in pancreatic cancer cells (BxPC-3, PANC-1) compared with HPDE6-C7. D, E The expression level of SH3BP5-AS1when ALKBH5 was overexpressed or silenced. F The relationship between ALKBH5 and SH3BP5-AS1 was confirmed by the luciferase reporter assay. G, H RIP RT-qPCR results showing the m6A modification level of SH3BP5-AS1 when ALKBH5 was overexpressed or silenced. I SH3BP5-AS1 stability analysis in BxPC-3 cells with ALKBH5 overexpression or knockdown in the presence of actinomycin D. J The negative correlation between the levels of IGF2BP1 and SH3BP5-AS1 in pancreatic cancer cells. K The enrichment of IGF2BP1 on SH3BP5-AS1 in pancreatic cancer cells was analyzed by RIP RT-qPCR assay. L, M The expression level of SH3BP5-AS1 when IGF2BP1 was overexpressed or knocked down. N Actinomycin D assays showing the effects of ALKBH5 overexpression or knockdown on IGF2BP1 stability. O RIP RT-qPCR assay results showing the enrichment of IGF2BP1 on SH3BP5-AS1 upon ALKBH5 silencing. Data are shown as the mean ± SD. *P < 0.05; **P < 0.01

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