Extended Data Fig. 6: The epigenetic reprogramming in SCLC with Kmt2c loss. | Nature Cancer

Extended Data Fig. 6: The epigenetic reprogramming in SCLC with Kmt2c loss.

From: KMT2C deficiency promotes small cell lung cancer metastasis through DNMT3A-mediated epigenetic reprogramming

Extended Data Fig. 6

(a) The levels of H3K4me1 bound at the enhancer (left) and TSS (right) in the PRM and PRMK SCLC cells, measured by CUT&Tag analyses. (b) Genome-wide distribution of the H3K4me1 up-regulated genes (left) and down-regulated genes (right) in PRMK compared to PRM, measured by CUT&Tag analyses. (c) The levels of H3K4me2 bound at the TSS in the PRM and PRMK SCLC cells, measured by CUT&Tag analyses. (d) Genome-wide distribution of the H3K4me2 up-regulated genes (left) and down-regulated genes (right) in PRMK compared to PRM, measured by CUT&Tag analyses. (e) The levels of H3K4me3 bound at the TSS in the PRM and PRMK SCLC cells, measured by CUT&Tag analyses. (f) Genome-wide distribution of the H3K4me3 up-regulated genes (left) and down-regulated genes (right) in PRMK compared to PRM, measured by CUT&Tag analyses. (g) The levels of ATAC bound at the TSS in the PRM and PRMK SCLC cells, measured by CUT&Tag analyses. (h) Genome-wide distribution of the ATAC open genes (top) and close genes (bottom) in PRMK compared to PRM. (i) The levels of KMT2C bound at the peaks of gene body in the PRM, PRM-Met and PRMK tumor cells, measured by the CUT& Tag analyses. (j) Genome-wide distribution of the KMT2C binding peaks in PRM, measured by CUT&Tag analyses.

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