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Analysis of the roles of AP4 and p53 downstream of c-MYC activation in breast cancer cells.

ABSTRACT: Deregulated expression of the c-MYC oncogene induces unscheduled DNA replication, DNA damage, and activation of the p53 tumor suppressor. The AP4 transcription factor is a direct c-MYC target gene involved in cell proliferation, epithelial-mesenchymal transition, and stemness, as well as suppression of DNA damage and senescence. Here, we analyzed the role of AP4 and p53 downstream of c-MYC activation using a CRISPR/Cas9-approach in MCF-7 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE221265 | GEO | 2023/03/01

REPOSITORIES: GEO

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Gene expression analysis of cMyc-deficient CD8 T cells retrovirally overexpressing cMyc or AP4

Project description:To determine functional overlap between cMyc and AP4 in CD8+ T cell priming, we retrovirally expressed cMyc or AP4 in cMyc-deficient CD8+ T cells and examined gene expression after activation. Naive CD8+ T cells from Myc conditional knockout mice with a tamoxifen inducible Cre transgene were retrovirally transduced with Myc or AP4 followed by a treatment with 4-hydroxytamoxifen in the presence of IL-7 for 2 days. RNA was harvested 48 hours after restimulation of transduced cells with anti-CD3 antibody and gene expression was compared by microarray. CD8+ T cells from littermate wildtype mice that were transduced with an empty retrovirus were used as control.

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Genome-wide mapping of Myc, AP4, and phosphorylated RNA polymerase II binding in activated CD8 T cells by ChIP sequencing

Project description:The trasncription factor cMyc is an essential transcription factor that establishes a metabolically active and proliferative state in T cells after antigen priming. However, its expression is transient. To date, it remains unknown how T cell activation is maintained after cMyc down-regulation. Here, we identify AP4, encoded by the gene Tfap4, as the transcription factor that is induced by cMyc and sustains activation of antigen-specific CD8+ T cells. Despite normal priming, Tfap4–/– CD8+ T cells fail to continue transcription of a broad range of cMyc gene targets necessary for sustained proliferation. Genome-wide analysis suggests that many activation-induced metabolic genes are shared targets of cMyc and AP4. Thus, AP4 maintains Myc-initiated cellular activation programs in CD8+ T cells to control microbial infections. Naive CD8+ T cells from C57BL6 mice were activated with anti-CD3 and anti-CD28 stimulation in vitro for two days and genome-wide occupancy of Myc, AP4 and Ser2 or Ser5 phipsphorylated RNA polymerase II was profiled by chromatin immunoprecipitation and high-throughput sequencing.

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Analysis of the roles of AP4 and p53 downstream of c-MYC activation in breast cancer cells.

Project description:Analysis of the roles of AP4 and p53 downstream of c-MYC activation in breast cancer cells.

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Defining AP4- and MYC-regulated gene expression programs in germinal center B cells during cyclic re-entry

Project description:B cells diversify and affinity-mature their antigen receptor repertoire in germinal centers (GC). GC B cells receive help signals during transient interaction with T cells, yet it remains unknown how these transient T-B interactions sustain the subsequent proliferative program of selected B cells. Here we show that the transcription factor AP4 is required for sustained GC B cell proliferation and subsequent establishment of a diverse and protective antibody repertoire. AP4 is induced by c-MYC during the T-B interactions and maintained by T cell-derived IL-21. B cell-specific deletion of AP4 resulted in reduced GC sizes and somatic hypermutation and a failure to control chronic viral infection. These results indicate that AP4 integrates T cell-mediated selection and sustained expansion of GC B cells for humoral immunity. Splenic B cells activated with anti-IgM and CD40L in vitro and germinal center B cells sorted from C57BL/6 mice eight days after immunization with sheep red blood cells (SRBCs) were obtained and genome-wide occupancy of c-MYC, AP4 and active histone marks was profiled by chromatin immunoprecipitation and high-throughput sequencing. Gene expression in MYCâAP4â LZ, MYC+AP4+ LZ, AP4+ DZ, and APâ DZ GC B cells from SRBC-immunized AP4-mCherry / c-MYC-GFP dual reporter mice was profiled by RNA-seq.

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