Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA138163 | ENA |
REPOSITORIES: ENA
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Project description:ES cells are able to self-renew and remain pluripotent. These characteristics are maintained by both genetic and epigenetic regulators. Protein arginine methyltransferase (PRMT) 4 and 5 are shown to be important in early embryonic development and in ES cells. PRMT6-mediated di-methylation of histone H3 at arginine 2 (H3R2me2) can antagonize the tri-methylation of histone H3 at lysine 4, which marks active genes. However, it is unclear whether PRMT6 and PRMT6-mediated H3R2me2 play crucial roles in early embryonic development and ES cell identity. In this study, we investigate their functions using mouse ES cells as the model. We used microarray (Affymetrix GeneChip Mouse Gene 1.0ST) to examine the global change of gene expression in mouse ES cells when Prmt6 was overexpressed and identified distinct classes of genes that are up-regulated and down-regulated during this process. Mouse ES cells were transfected with either pCAGIP.puro empty vector (control) or Prmt6 overexpressing plasmid (P+6 OE). After 3 days of selection by puromycin, cells from both populations were subjected to RNA extraction and hybridization on Affymetrix microarrays.
2011-03-04 | E-GEOD-27685 | biostudies-arrayexpress
Project description:ES cells are able to self-renew and remain pluripotent. These characteristics are maintained by both genetic and epigenetic regulators. Protein arginine methyltransferase (PRMT) 4 and 5 are shown to be important in early embryonic development and in ES cells. PRMT6-mediated di-methylation of histone H3 at arginine 2 (H3R2me2) can antagonize the tri-methylation of histone H3 at lysine 4, which marks active genes. However, it is unclear whether PRMT6 and PRMT6-mediated H3R2me2 play crucial roles in early embryonic development and ES cell identity. In this study, we investigate their functions using mouse ES cells as the model. We used microarray (Affymetrix GeneChip Mouse Gene 1.0ST) to examine the global change of gene expression in mouse ES cells when Prmt6 was overexpressed and identified distinct classes of genes that are up-regulated and down-regulated during this process.
2011-03-04 | GSE27685 | GEO
Project description:Illumina Beadchip array analyses of mouse embryonic stem cell gene expression profiles upon knockdown of Prmt6 vs GFP control.
2019-11-26 | GSE33635 | GEO
Project description:Purpose: Dysregulation of histone H3 arginine (R) methylation is still unknown in primary cancer including gastric cancer (GC), although PRMT6 plays a role in asymmetric dimethylation at H3R2 (H3R2me2as) in cancer cells. The objective is to clarify biological and molecular roles of H3R2me2as-PRMT6 pathway in GC. Experimental Design: We assessed H3R2me2as and PRMT6 levels in 133 primary GC tissues by immunohistochemistry. We analyzed biological functions of PRMT6 in GC cell lines using a lentivirus overexpression and CRISPR/Cas9-based knockout of PRMT6 systems. Results: Increased H3R2me2as was found in 68 GC (51.1%) cases and independently correlated with poor prognosis. PRMT6 was overexpressed in 70 (52.6%) GC, which strongly correlated with the H3R2me2as levels (P<0.001). PRMT6 overexpression in GC cells enhanced global H3R2me2as levels, cell invasiveness in vitro, while PRMT6-knockout GC cells suppressed these effects. PRMT6 knockout also impaired tumorigenicity in vivo. Microarray and ChIP assays demonstrated that PRMT6-knockout GC cells decreased the H3R2me2as levels at the promoter regions of PCDH7, SCD and IGFBP5, resulting in up-reregulation of their gene expression. PRMT6 recruited at the regions of PCDH7 and SCD in the PRMT6-overexpressed cells. Knockdown of tumor suppressor PCDH7 in PRMT6-knockout GC cells elevated cell migration and invasion. PRMT6 expression inversely correlated with PCDH7 expression in primary GC (P=0.021). Conclusions: H3R2me2as is a strong prognostic indicator of GC patients. Global and gene-specific H3R2me2as are maintained by PRMT6. PRMT6-overexpressed GC cells may acquire invasiveness through direct inhibition of PCDH7 by increasing H3R2me2as activity. Thus, PRMT6-H3R2me2as pathway is a promising new therapeutic target in GC.
2020-04-16 | GSE113188 | GEO
Project description:Purpose: Dysregulation of histone H3 arginine (R) methylation is still unknown in primary cancer including gastric cancer (GC), although PRMT6 plays a role in asymmetric dimethylation at H3R2 (H3R2me2as) in cancer cells. The objective is to clarify biological and molecular roles of H3R2me2as-PRMT6 pathway in GC. Experimental Design: We assessed H3R2me2as and PRMT6 levels in 133 primary GC tissues by immunohistochemistry. We analyzed biological functions of PRMT6 in GC cell lines using a lentivirus overexpression and CRISPR/Cas9-based knockout of PRMT6 systems. Results: Increased H3R2me2as was found in 68 GC (51.1%) cases and independently correlated with poor prognosis. PRMT6 was overexpressed in 70 (52.6%) GC, which strongly correlated with the H3R2me2as levels (P<0.001). PRMT6 overexpression in GC cells enhanced global H3R2me2as levels, cell invasiveness in vitro, while PRMT6-knockout GC cells suppressed these effects. PRMT6 knockout also impaired tumorigenicity in vivo. Microarray and ChIP assays demonstrated that PRMT6-knockout GC cells decreased the H3R2me2as levels at the promoter regions of PCDH7, SCD and IGFBP5, resulting in up-reregulation of their gene expression. PRMT6 recruited at the regions of PCDH7 and SCD in the PRMT6-overexpressed cells. Knockdown of tumor suppressor PCDH7 in PRMT6-knockout GC cells elevated cell migration and invasion. PRMT6 expression inversely correlated with PCDH7 expression in primary GC (P=0.021). Conclusions: H3R2me2as is a strong prognostic indicator of GC patients. Global and gene-specific H3R2me2as are maintained by PRMT6. PRMT6-overexpressed GC cells may acquire invasiveness through direct inhibition of PCDH7 by increasing H3R2me2as activity. Thus, PRMT6-H3R2me2as pathway is a promising new therapeutic target in GC.
2020-04-16 | GSE113189 | GEO
Project description:Histone modification, a major epigenetic mechanism which regulates gene expression by chromatin remodeling, introduces dynamic changes in chromatin architecture. Protein arginine methyltransferase 6 (PRMT6) is overexpressed in various types of cancers. Epigenome regulates the expression of endogenous retrovirus (ERV), which activates interferon signaling related to cancer. We investigated the antitumor effects of PRMT6 inhibition and the role of PRMT6 in endometrial cancer (EC), using epigenome multi-omics analysis including assay for chromatin immunoprecipitation sequencing (ChIP-seq) and ribonucleic acid sequencing (RNA-seq). The expression of PRMT6 in EC was analyzed using real-time quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC). The prognostic impact of PRMT6 expression was evaluated using IHC. We investigated the effects of PRMT6-knockdown (KD) using cell viability and apoptosis assays, as well as its effects on the epigenome using ChIP-seq of H3K27ac antibodies and RNA-seq. Finally, we evaluated the downstream targets identified by multi-omics analysis. PRMT6 was overexpressed in EC and associated with a poor prognosis. PRMT6-KD induced histone hypomethylation, while suppressing cell growth and apoptosis. ChIP-seq revealed that PRMT6 regulated genomic regions related to interferons and apoptosis through histone modifications. RNA-seq data showed altered interferon-related pathways and increased expression of tumor suppressor genes, such as NKX6-1 and PIK3R1, after PRMT6-KD. RT-qPCR showed that eight ERV genes which activated interferon signaling were upregulated by PRMT6-KD. Our data suggested that PRMT6 inhibition induced apoptosis through interferon signaling activated by ERV. PRMT6 regulated tumor suppressor genes and may be a novel therapeutic target in EC.
2024-02-07 | GSE239295 | GEO
Project description:Histone modification, a major epigenetic mechanism which regulates gene expression by chromatin remodeling, introduces dynamic changes in chromatin architecture. Protein arginine methyltransferase 6 (PRMT6) is overexpressed in various types of cancers. Epigenome regulates the expression of endogenous retrovirus (ERV), which activates interferon signaling related to cancer. We investigated the antitumor effects of PRMT6 inhibition and the role of PRMT6 in endometrial cancer (EC), using epigenome multi-omics analysis including assay for chromatin immunoprecipitation sequencing (ChIP-seq) and ribonucleic acid sequencing (RNA-seq). The expression of PRMT6 in EC was analyzed using real-time quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC). The prognostic impact of PRMT6 expression was evaluated using IHC. We investigated the effects of PRMT6-knockdown (KD) using cell viability and apoptosis assays, as well as its effects on the epigenome using ChIP-seq of H3K27ac antibodies and RNA-seq. Finally, we evaluated the downstream targets identified by multi-omics analysis. PRMT6 was overexpressed in EC and associated with a poor prognosis. PRMT6-KD induced histone hypomethylation, while suppressing cell growth and apoptosis. ChIP-seq revealed that PRMT6 regulated genomic regions related to interferons and apoptosis through histone modifications. RNA-seq data showed altered interferon-related pathways and increased expression of tumor suppressor genes, such as NKX6-1 and PIK3R1, after PRMT6-KD. RT-qPCR showed that eight ERV genes which activated interferon signaling were upregulated by PRMT6-KD. Our data suggested that PRMT6 inhibition induced apoptosis through interferon signaling activated by ERV. PRMT6 regulated tumor suppressor genes and may be a novel therapeutic target in EC.
2024-02-07 | GSE239294 | GEO
Project description:Mouse embryonic stem (ES) cells are locked into self-renewal by shielding from inductive cues. Release from this ground state in minimal conditions offers a system for delineating developmental progression from naive pluripotency. Here we examined the initial transition process. The ES cell population behaves asynchronously. We therefore exploited a short-half-life Rex1::GFP reporter to isolate cells either side of exit from naive status. Differentiation of Rex1-GFPd2 ES cells was initiated by withdrawing 2i (Kalkan et al., 2016). Undifferentiated 2i-cells and post-2i withdrawal differentiating populations (16h, 25h-Rex1-High, 25h-Rex1-Low) were subjected to proteomic analysis by Mass Spectrometry.
2017-02-22 | PXD005581 | Pride
Project description:Our understanding of the biology of embryonic stem (ES) cells is deeply rooted in characterization of their transcriptomes, epigenetics and underlying gene regulatory networks. There is evidence that post-transcriptional processes such as signaling, adhesion, protein turnover and post translational modifications make a significant contribution to regulating the balance between self-renewal and differentiation, and it is therefore necessary to also characterize ES cells at the protein level. In this experiment, we used a workflow termed hyperLOPIT (hyperplexed localization of organelle proteins by isotope tagging) to characterize the subcellular distribution of proteins in a population of self-renewing E14TG2a mouse ES cells. Over 5,000 protein groups were quantified in both of the two replicates, enabling characterization of protein localization to organelles (including sub-nuclear resolution), cell surface, cytoskeleton and cytosol. The steady-state localization of transitory proteins, protein complex constituents, and signaling cascades could also be mapped.
2016-01-14 | PXD001279 | Pride
Project description:Expression data from mouse germline stem (GS), multipotent germline stem (mGS), and embryonic stem (ES) cells.
| PRJNA107783 | ENA