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. 2019 Jan 21;20(3):e46821. doi: 10.15252/embr.201846821

Figure 4. KMT2C controls the expression of DDR and DNA repair genes in various cancers.

Figure 4

  1. Bedgraphs indicating KMT2C and H3K4me3 binding at the TSS of indicated loci in HTB9 cells; also, from published studies available at the ENCODE, the binding of the COMPASS complex member RBBP5 and the transcription factor ELK1 is indicated in the same loci.
  2. KMT2C expression (y‐axis) in various human cell lines (x‐axis). Cell lines under study are indicated as red geometrical schemes. Data were obtained directly from the Broad Institute CCLE server.
  3. Expression levels of indicated genes in indicated cell lines upon KMT2C knockdown. Expression is shown as log(KD1/Scr) in the y‐axis. Remaining KMT2C transcript levels for all knockdown experiments can be found in Table EV2. Note that H1792 which shows poor KD1 (˜25%) also shows no change in ATM, ATR, BRCA1, and BRCA2 expression (light red bar appearing last in each set). Experiments were performed in triplicates. In plots, bars represent mean ± SEM.
  4. Correlation in expression levels between KMT2C and indicated genes in our study cohort of superficial and muscle‐invasive BC. Data obtained from qRT–PCR. Experiments were performed in duplicates. P values were calculated by Mann–Whitney U‐test.
  5. Correlation in expression levels between KMT2C and indicated genes in BC, COAD, NSCLC, and HNSCC tumors. RNA‐seq data were obtained from the TCGA through cbioportal.org. Mann–Whitney U‐test was used. *** designates P‐value < 0.001 and ****P‐value < 0.0001.