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. 2022 Dec 15;108(7):1886–1899. doi: 10.3324/haematol.2022.281444

Figure 1.

Figure 1.

CCRL2 knockdown downregulates pathways associated with DNA methylation and PRC2 activity. (A) RNA sequencing and gene set enrichment analysis in RNA collected from TF-1 cells transduced with shControl or shCCRL2 (sh1) lentiviruses and selected with puromycin demonstrated a number of oncogenic pathways downregulated by CCRL2 knockdown (KD). Among the topdownregulated pathways were pathways associated with DNA methylation and PRC2 activity. (B) Enrichment plots showing the suppression of PRC2 methylation activity and DNA methylation pathways by CCRL2 KD. (C) Western blot showing that CCRL2 KD suppressed DNMT3A and DNMT3B in TF-1 cells and all the DNMT in MDS-L cells. CCRL2 KD also increased p27 levels, decreased RB1 phosphorylation, and suppressed the protein levels of the PRCA component SUZ12, and the TFRC targets LIN28B and GNAQ in both TF-1 and MDS-L cells. CCRL2 KD decreased the nuclear levels of E2F1 in both TF-1 and MDS-L cells. (D) Box plot of normalized expression of selected genes encoding DNA methyltransferases (DNMT) and PRC2 components between CCRL2 knockout cells and controls. NES: normalized enrichment score; FDR: false discovery rate.