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. 2022 Aug 9;8:354. doi: 10.1038/s41420-022-01125-y

Fig. 6. Down-regulated FTO/PHF1 axis enhanced the tumor self-renewal capacity and tumor progression in vitro and in vivo.

Fig. 6

A Gene set enrichment analysis (GSEA) was conducted to compare the enriched pathways in PHF1-low and PHF1-high groups. B Tumorsphere images of LUAD CSCs in parental WT and PHF1-KO groups (Scale bar = 200 μm). Quantification was shown on the right. C In vitro limiting dilution analysis of the tumorsphere formations of LUAD CSCs (WT & KO#1). PHF1 deficiency enhanced the self-renewal capacity of LUAD CSCs. D The qPCR assay screening the representative stemness-associated signature in parental and PHF1-KO A549 cells. E The qPCR assay detecting the FOXM1 mRNA levels in LUAD cells (A549, H1299) transfected with vetctor and PHF1. F ChIP-qPCR assays were performed to detect the enrichment of PHF1 and corresponding H3K36me3 at the promoter loci of FOXM1. G Gene correlation analysis was conducted with Spearson statistics between PHF1 and FOXM1 based on the TCGA-LUAD cohort. H CCK-8 assay was conducted to detect the in vitro cell growth in PHF1-deficient cells infected with shCtrl or shFOXM1. I The qPCR assay was conducted to detect the relative FOXM1 mRNA levels in FTO-KD cells transfected with vector or PHF1. J CCK-8 assay was performed to detect the in vitro cell growth in FTO-KD cells infected with shCtrl or shFOXM1. K Representative images of mice with xenografts tumors derived from H1299 cells. L Quantification of tumor volumes at indicated timepoints in the above subcutaneous model. Bar = Mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.