Analysis of KMT2D Knockdown/Control PC-3 Cell Line
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ABSTRACT:
PROVIDER: PRJNA374508 | ENA |
REPOSITORIES: ENA
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Project description:KMT2D is a histone methyltransferase for catalyzing the monomethylation of H3K4. Previous studies have indentified that H3K4me1 is prominent on active enhancers and participates in gene expression regulation. To further examine the transcriptional changes in response to KMT2D depletion, we performed RNA-seq with KMT2D knockdown and control PC-3 cells by BGISEQ-500
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Project description:KMT2D is a histone methyltransferase for catalyzing the monomethylation of H3K4. The H3K4me1 is prominent on active enhancers and participates in gene expression regulation. Loss of KMT2D in cancer has been approved to impact on a set of gene expression by the reduction of H3K4me1 level. To identify the direct target of KMT2D in prostate cancer, we performed H3K4me1 ChIP-seq with KMT2D knockdown and control PC-3 cells.
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Project description:This SuperSeries is composed of the SubSeries listed below.
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Project description:Define and compare H3K4me2 enrichment in murine B220 cells transduced with empty vector (ct) or KMT2D-shRNA. Compare gene expression by RNAseq in murine B220 cells transduced with empty vector (ct) or KMT2D-shRNA. Using H3K4me1/2 ChIPseq and RNAseq we profiled murine B220 purified cells from tumors transduced with EV (n=3) or KMT2D-shRNA (n=3).
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Project description:To identify the genes associated with the knockdown of ELL2. PC-3 mRNA profiles of cells treated with RNA interference ELL2 compared to non-targeted control siRNA were tested using RNA seq. RNA isolation was performed using RNeasy Plus Mini kit. In this study, we identified 1939 differentially expressed genes associated with ELL2 deletion. Of these transcripts,1579 genes involve in cancer, while 695 genes are asscoicated with cell death and survival. Bioinformatics analysis indicated that ELL2 knockdown activates the IFNγ-STAT1-IRF1 signaling pathway, which is known to play important roles in prostate cancer.
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Project description:Next Generation Sequencing Facilitates Quantitative Analysis of KMT2D Knockdown/Control PC-3 Cell Line Transcriptomes
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Project description:Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide, with 5-year survival of ~50%. Genomic profiling studies have identified important somatic mutations in this disease which presents an opportunity for precision medicine. We demonstrate that KMT2D, a histone methyltransferase harbors somatic mutations in ~17% of HNSCC and is associated with 2-year recurrence in TCGA data. Consistent with algorithmic prediction of bring a driver tumor-suppressor event, its loss results in larger oral tumors in immune-proficient orthotopic models. Mechanistically, we find that KMT2D knockdown or KMT2D mutation causes loss of H3K4me1-marked enhancers harboring IRF7/9 binding sites, which is known to regulate interferon signaling. Indeed, KMT2D loss in human and murine cell lines deregulated transcriptional levels of cytokine expression and impacted numerous immune signaling pathways, including interferon signaling. Consistently, Kmt2d knockdown in murine tumors exhibited decrease in IFN-producing effector T cells and an increase in T-cells with an exhausted phenotype. Epistasis experiments showed that exogenous treatment with IFNabrogated the increased tumor growth in Kmt2d-deficient oral tumors. Together, these results support the role of KMT2D as a tumor suppressor in HNSCC that regulates the tumor microenvironment by modulating H3K4me1-marked enhancers controlling interferon signaling.
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Project description:Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide, with 5-year survival of ~50%. Genomic profiling studies have identified important somatic mutations in this disease which presents an opportunity for precision medicine. We demonstrate that KMT2D, a histone methyltransferase harbors somatic mutations in ~17% of HNSCC and is associated with 2-year recurrence in TCGA data. Consistent with algorithmic prediction of bring a driver tumor-suppressor event, its loss results in larger oral tumors in immune-proficient orthotopic models. Mechanistically, we find that KMT2D knockdown or KMT2D mutation causes loss of H3K4me1-marked enhancers harboring IRF7/9 binding sites, which is known to regulate interferon signaling. Indeed, KMT2D loss in human and murine cell lines deregulated transcriptional levels of cytokine expression and impacted numerous immune signaling pathways, including interferon signaling. Consistently, Kmt2d knockdown in murine tumors exhibited decrease in IFN-producing effector T cells and an increase in T-cells with an exhausted phenotype. Epistasis experiments showed that exogenous treatment with IFNabrogated the increased tumor growth in Kmt2d-deficient oral tumors. Together, these results support the role of KMT2D as a tumor suppressor in HNSCC that regulates the tumor microenvironment by modulating H3K4me1-marked enhancers controlling interferon signaling.
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Project description:We identified KMT2D target loci in OCI-LY7 by ChIPseq. KMT2D ChIPseq was carried out in the LY7 cell line (n=1).
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