Editorial
Copyright ©The Author(s) 2020.
World J Immunol. May 27, 2020; 10(1): 1-12
Published online May 27, 2020. doi: 10.5411/wji.v10.i1.1
Figure 1
Figure 1 A schematic model showing the two distinct polycomb repressive complex 2 complexes and the potential alteration of their transcriptional repression activity by protein kinase C-interacting protein cousin of thioredoxin interaction with embryonic ectoderm development. Each of the two complexes possesses the same four core subunits, including embryonic ectoderm development (EED), suppressor of zeste12, RbAp46 (or RbAp48) and enhancer of zeste homolog 2 or 1 (EZH2 or EZH1), and is responsible for the mono-, di-, and tri-methylation of lysine 27 on histone H3 (H3K27me1/2/3) on chromatin. The polycomb repressive complex 2.1 (PRC2.1) complex is defined by its association with the Pcl1-3 and Pali1/2 auxiliary proteins, while PRC2.2 associates with Aebp2 and Jarid2. The two antagonistic PRC2 complexes exhibit divergent methyltransferase activities, they regulate the repression of different sets of polycomb target genes, and the balance between them is essential for the proper regulation of gene transcription. Recent findings demonstrated that protein kinase C-interacting protein cousin of thioredoxin (PICOT) association with EED can alter the transcription of certain PRC2 target genes, suggesting the involvement of PICOT in PRC2-dependent transcriptional regulation. A differential interaction of PICOT with PRC2.1- or PRC2.2-associated EED might have different impacts on cellular epigenetic mechanisms that alter distinct cell-specific gene expression signatures. Aebp2: Adipocyte enhancer-binding protein 2; EED: Embryonic ectoderm development; SUZ12: Suppressor of zeste 12; EZH2: Enhancer of zeste homolog 2; H3K27: Histone 3 lysine 27; Jarid2: Jumonji and AT-rich interaction domain containing 2; me3: tri-methyl; Pali1: PRC2-associated LCOR isoform 1; Pcl1: Polycomb-like proteins 1; PICOT: Protein kinase C-interacting protein cousin of thioredoxin; PRC2: Polycomb repressive complex-2; RbAp46: Retinoblastoma protein-associated protein 46; SUZ12: Suppressor of Zeste 12.
Figure 2
Figure 2 High expression of PICOT and low expression of CCND2 correlate with poor patient survival in different types of human cancer. PICOT and CCND2 mRNA expression and cancer patients’ clinical data were derived from the Cancer Genome Atlas database. Patients were divided into high or low expression groups, using the maximally selected rank statistics that is implemented in the R package “survminer”. Survival of patients was visualized using the Kaplan–Meier estimator and the 5 years survival probability of lung adenocarcinoma and 2 years survival probability of pancreatic adenocarcinoma, esophageal carcinoma and glioblastoma multiforme were calculated and presented in the bar graph.