Leukemia dynamics and heterogeneity traced by barcoding in a pre-clinical Cbx7 mouse model
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE56820 | GEO | 2014/10/01
SECONDARY ACCESSION(S): PRJNA244677
REPOSITORIES: GEO
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Project description:Polycomb CBX7 was stably expressed in embryonal carcinoma cells in order to identify target genes. The study was specifically geared toward unveiling gene targets that are susceptible to DNA hypermethylation in adult cancer. A number of CBX7 target tumor suppressor genes were thereby identified and used in further studies to characterize the mechanism surrounding CBX7 mediated gene suppression. Keywords: CBX7 target gene identification A cDNA encoding the ORF of polycomb CBX7 under the control of EF1alpha promoter was transfected into the Tera-2 embryonal carcinoma cell line. Empty vector was used to transfect control cells. The cells were subject to stable selection using puromycin and a pooled population of CBX7 overexpressing cells was established. Gene expression analysis was performed by comparing the gene expression profile of CBX7 cells to empty vector control cells.
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Project description:The Polycomb Group Proteins (PcG) are epigenetic regulatory complexes, dysregulation of which has been associated with multiple biological processes, including maintenance of cell identity, differentiation, proliferation, and cancer progression.PcGs form two multiprotein complexes, Polycomb repressive complex 1 (PRC1) and PRC2(1).The PRC2 protein complex mainly consists of Early embryonic deficient (EED), Suppressor of Zeste (SUZ12) and Enhancer of Zeste (EZH), which can catalyzes the trimethylation of histone H3 lysine 27 (H3K27me3), thereby leaving a transcriptionally repressive mark on the chromatin . Such alterations are recognized and read by canonical PRC1 which is composed of CBX (polycomb), PCGF (polycomb group factor), HPH (human polyhomeotic homolog), and the E3-ligase protein (RING) that catalyzes the monoubiquitination of histone H2A on lysine 119 (H2AK119ub1). The H3K27me3 mark is identified by and binds to the chromodomain within the CBX protein in PRC1, thereby ubiquitinating H2AK119 via the RING proteins. The interaction of PRC2 and PRC1 in chromatin contributes to chromatin compaction and transcriptional silencing of target genes.There are five chromobox proteins in humans, CBX2, 4, 6, 7 and 8. Increasing evidence supports essential roles of CBX proteins in tumorigenesis. Remarkably, CBX proteins have shown an opposite function in distinct cancer types in tumor development. For example, CBX7 is overexpressed in ovarian and prostate cancer , implying its oncogenic role in these tumor types. In contrast, CBX7 functions as a tumor suppressor and loss of CBX7 has been associated with increasing the malignancy grade in bladder, breast, pancreatic, glioma, and colon carcinomas (3 4 5 6 7), but its tumor suppression mechanism is unclear.
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Project description:Purpose: miR-181 is upregulated in human liver cancer. The cancer genome atlas (TCGA) liver cancer data show that the iCluster1 subclass of hepatocellular carcinoma (HCC) has a higher expression of miR-181 than either the iCluster2 or iCluster3 subclass, suggesting it may be a driver of oncogenesis. However, the miR-181 family has also been reported to inhibit tumour progression. Thus, we aim to examine the function of miR-181 and its vital mediators in hepatocarcinogenesis. Methods: Primary liver tumours were induced with diethylnitrosamine (DEN) in global (miR-181ab1GKO), liver-specific (miR-181ab1LKO) and hematopoietic & endothelial lineage-specific (miR-181ab1vavKO) miR-181ab1 deletion mice. The molecular and cellular characterization was carried out using immunohistochemistry and whole-genome transcriptome analysis. Liver-specific miR-181a and CBX7 double knockout mice were used to investigate the role of CBX7 in mediating miR-181 effects on liver tumour progression. An AAV/Transposase Hybrid-Vector System used in this study gave a reliable long-term expression of CBX7 in vivo. Relevant gene expression profiles and patient outcomes were downloaded from TCGA database, and their correlations were analysed. The mRNA profiles of miR-181ab1 wild-type (WT) and knockout (KO) mice were generated by deep sequencing, in triplicate, using Illumina HiSeq. After quality control procedures, short reads were mapped to mouse genome assembly (mm10) by STAR version 2.7.3a. Mapped reads were quantified by featureCounts version 2.0.0 from Subread package. Ward’s hierarchical clustering method was applied to group the samples based on the gene expression matrix. Differential gene expression analysis was then conducted using R package Limma. Gene set enrichment analysis was subsequently performed with R package clusterProfiler. Overlaps between differential expressed gene sets and gene sets in MSigDB were computed with Gene Set Enrichment Analysis (GSEA). Results: The number and size of liver tumours in 181ab1GKO mice were significantly reduced by 50% and 90%, respectively, compared to WT mice at 34-week post-DEN injection. The number of tumours in 181ab1LKO mice was no different from that of control mice, but the size of liver tumours was significantly reduced by 90%. The number and size of tumours were similar in miR-181ab1vavKO and WT mice. Consistent with the roles of miR-181 in the promotion of epithelial to mesenchymal transition (EMT), the TGF-beta signalling pathway was inhibited in 181ab1GKO tumours compared with WT tumours, and expression of E-Cadherin, an EMT marker, was significantly increased in miR-181ab1 KO tumours compared to WT tumours. CBX7 was reduced in WT liver tumours compared to non-tumours, and restored CBX7 expression inhibited the progression of liver tumours in WT mice. At the same time, CBX7 was upregulated in miR-181ab1 KO tumours compared to WT tumours, and CBX7 deletion turned the reduced progression of miR-181ab1 KO liver tumours back to WT liver tumours. MiR-181a expression was the lowest and CBX7 expression the highest in iCluster 2 & 3 subclasses of human HCC compared to iCluster 1. Gene expression profiles were significantly overlapped between human low proliferative periportal-type HCCs and miR-181ab1 KO tumours. Conclusions: Primary liver tumour progression is inhibited by loss of miR-181ab1 via up-regulation of CBX7 expression at the level of the liver cancer cells themselves, but tumour induction requires both hepatic and non-hepatic expression. Tumours in miR-181ab1 KO mice resemble low-proliferative periportal-type human HCC and could represent a new model to study therapies for such difficult-to-treat tumours.
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