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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: MYCN and PRC1 cooperatively repress docosahexaenoic acid synthesis in neuroblastoma via ELOVL2

Fig. 3

MYCN recruits the PRC1 complex to the ELOVL2 promoter region and mediates ELOVL2 inhibition by H2AK119ub. a ChIP-Seq analysis from MYCN-amplified cell lines (NGP and BE(2)-C) and MYCN single-copy cell lines (SK-N-SH) using antibodies detecting MYCN (black bar) and H3K4me3 (blue and orange bar) superimposed on the ELOVL2 cluster genomic organization. b ChIP analysis in the IMR32 and BE(2)-C cell lysates showing MYCN recruitment to the ELOVL2 promoter region. c ChIP analysis in BE(2)-C cells stably expressing the negative control or ELOVL2 shRNA showing reduced H3K4me3 and H3K9ac enrichment, and increased H3K27me3 enrichment to the ELOVL2 promoter region. d BE(2)-C cell lysates immunoprecipitated with antibodies against MYCN were analysed using mass spectrometry to detect potential binding partner proteins of MYCN. The PRC1 complex consisting of BMI1, RING1A and RING1B was detected. e and f Western blots of BE(2)-C cell lysates coimmunoprecipitated with antibodies against MYCN, BMI1, RING1A and RING1B shown with the IgG control antibody and 1% of the lysate input to assess the PRC1-MYCN protein interaction. g qRT-PCR showing relative ELOVL2 mRNA expression (fold-change over negative control ± SD) in BE(2)-C cells 48 h after BMI1, RING1A or RING1B siRNA treatment. h ChIP analysis showing relative ELOVL2 promoter enrichment of H2AK119ub, RING1B and BMI1 in BE(2)-C cells treated as in (B). i ChIP analysis showing relative ELOVL2 promoter enrichment of MYCN in BE(2)-C cells 48 h after BMI1 or RING1B siRNA treatment. j ChIP analysis showing relative ELOVL2 promoter enrichment of SREBP1 in BE(2)-C cells treated as in (b) and (i). *P < 0.05; **P < 0.01

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