Fig. 7: KRAS activates HIF1A-As2 through MYC. | Cell Death & Differentiation

Fig. 7: KRAS activates HIF1A-As2 through MYC.

From: Long non-coding RNA HIF1A-As2 and MYC form a double-positive feedback loop to promote cell proliferation and metastasis in KRAS-driven non-small cell lung cancer

Fig. 7

A MYC gene signature is enriched in KRAS WT or KRAS G12D gene sets. B Immunoblotting showing upregulated MYC by overexpressed KRAS WT or KRAS G12D. C KRAS is significantly correlated with MYC in LUAD corhorts (GTex + LUAD = 965). D RT-qPCR for HIF1A-As2 level after silencing of MYC in H1299 and A549 cells. MALAT1 was used as a positive control. E CAGE-seq revealing the potential transcription start sites of HIF1A-As2. CAGE-seq counts were defined by FANTOM5 mammalian promoter expression atlas in H460 and A549 cells. Purple dashed lines show the start position and end position of HIF1A-As2. F UCSC Genome Browser showing the ChIP-seq signals of H3K4me3, H3K27ac and MYC on the HIF1A-As2 promoter locus. G MEME analysis for the binding motifs of transcription factor MYC on HIF1A-As2 promoter locus. H ChIP-qPCR showing the enrichment of MYC on HIF1A-As2 promoter in H1299 cells. H3K4me3 and H3K27ac were used as positive controls. I The induction of HIF1A-As2 by KRAS WT or KRAS G12D was abolished by MYC KD in BEAS2B (Left) and H1299 (Right) cells. D, H and I Data show mean ± S.D (n = 3). **p value < 0.001, *p value < 0.05 by two-tailed Student’s t test.

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