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Epigenetically-controlled tumor antigens derived from splice junctions between exons and transposable elements

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE218085 | GEO | 2022/11/22

REPOSITORIES: GEO

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Epigenetically-controlled tumor antigens derived from splice junctions between exons and transposable elements [RNA-seq]

Project description:To study the expression of junctions between exons and transposable elements (TEs), we generated paired-end RNAseq from various mouse tumor cell lines, with several biological replicates (cultures from different days). To analyse regulation of JET expression, we generated Setdb1-deficient B16F10 and B16OVA cells, using lentivirus-based CRISPR/Cas9. Ctrl and KO cells lines were used to generate paired-end RNAseq, with several biological replicates (cultures on different days). We generated paired-end RNAseq from healthy female mouse tissues, to compare JET expression in healthy and tumor cells.

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Epigenetically-controlled tumor antigens derived from splice junctions between exons and transposable elements [ChIP-seq]

Project description:To analyze regulation of JET expression, we generated Setdb1-deficient MC38 and B16OVA cells, using lentivirus-based CRISPR/Cas9. Ctrl and KO cells lines were used to perform ChIP-seq against H3K9me3 and H3K9Ac, with 3 biological replicates.

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Epigenetically-controlled tumor antigens derived from splice junctions between exons and transposable elements

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Epigenetically-controlled tumor antigens derived from splice junctions between exons and transposable elements [RNA-seq]

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Epigenetically-controlled tumor antigens derived from splice junctions between exons and transposable elements [ChIP-seq]

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Non-canonical splicing junctions between exons and transposable elements represent a source of immunogenic recurrent neo-antigens in cancer patients

Project description:ost characterized tumor antigens are ‘genomic’, i.e. encoded by canonical, non-canonical or somatically mutated genomic sequences. We investigate here the presentation and immunogenicity of tumor antigens derived from non-canonical mRNA splicing events between coding exons and transposable elements (TEs). Comparing non-small cell lung cancer (NSCLC), an immunogenic tumor type, and diverse non-tumor tissues, we identify several thousand splicing junctions between exons and diverse TE classes. A subset of these junctions is both tumor-specific and shared across patients. HLA-I peptidomic identifies peptides encoded by tumor-specific junctions in primary NSCLC samples and lung tumor cell lines. Recurrent junction-encoded peptides are immunogenic in vitro and CD8+ T cells specific for junction-encoded epitopes are present in tumors and tumor-draining lymph nodes from NSCLC patients. We conclude that non-canonical splicing junctions between exons and TEs represent a source of recurrent, immunogenic tumor-specific antigens in NSCLC cancer patients.

2023-02-27 | PXD034820 | Pride

Pan-cancer tumor-specific antigens and membrane targets from transposable elements

Project description:Cryptic promoters within transposable elements (TEs) are transcriptionally reactivated in tumors to create novel TE-gene chimeric transcripts, which can produce immunogenic antigens. We performed the most comprehensive screen to date for these TE exaptation events in 33 TCGA tumor types, 675 cancer cell lines, and 11,686 GTEx adult tissue transcriptomes and identified 1,068 TE-exapted candidates with the potential to generate shared tumor-specific TE-chimeric antigens (TS-TEAs). Resultant whole lysate and HLA-pulldown mass spectrometry data confirmed that TS-TEAs are presented on cancer cell surfaces. In addition, we highlight the tumor-specific membrane proteins transcribed from TE promoters that can expose novel epitopes on the extracellular surface of cancer cells. Here, we showcase the high pan-cancer prevalence of TS-TEAs and atypical membrane proteins that can be therapeutically exploited through immunotherapy approaches.

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Pan-cancer tumor-specific antigens and membrane targets from transposable elements

Project description:We charted the transcription start sites (TSSs) landscape globally to determine the expressed isoform of each gene and validate the precence of transposable element-derived transcript. Cryptic promoters within transposable elements (TEs) are transcriptionally reactivated in tumors to create novel TE-gene chimeric transcripts, which can produce immunogenic antigens. We performed the most comprehensive screen to date for these TE exaptation events in 33 TCGA tumortypes,675 cancer cell lines, and 11,686 GTEx adult tissue transcriptomes and identified 201,068 TE-exapted candidates with the potential to generate shared tumor-specific TE-chimeric antigens (TS-TEAs). Resultant whole lysate and HLA-pull down mass spectrometry data confirmed that TS-TEAs are presented on cancer cell surfaces. In addition, we highlight the tumor-specific membrane proteins transcribed from TE promoters that can expose novel epitopes on the extracellular surface of cancer cells. Here, we showcase the high pan-cancer prevalence of TS-TEAs and atypical membrane proteins that can be therapeutically exploited through immunotherapy approaches.

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Translocation junctions in TCF3-PBX1 acute lymphoblastic leukemia/lymphoma cluster near transposable elements.

Project description:BackgroundHematolymphoid neoplasms frequently harbor recurrent genetic abnormalities. Some of the most well recognized lesions are chromosomal translocations, and many of these are known to play pivotal roles in pathogenesis. In lymphoid malignancies, some translocations result from erroneous V(D)J-type events. However, other translocation junctions appear randomly positioned and their underlying mechanisms are not understood.ResultsWe tested the hypothesis that genomic repeats, including both simple tandem and interspersed repeats, are involved in chromosomal translocations arising in hematopoietic malignancies. Using a database of translocation junctions and RepeatMasker annotations of the reference genome assembly, we measured the proximity of translocation sites to their nearest repeat. We examined 1,174 translocation breakpoints from 10 classifications of hematolymphoid neoplasms. We measured significance using Student's t-test, and we determined a false discovery rate using a random permutation statistics technique.ConclusionsMost translocations showed no propensity to involve genomic repeats. However, translocation junctions at the transcription factor 3 (TCF3)/E2A immunoglobulin enhancer binding factors E12/E47 (E2A) locus clustered within, or in proximity to, transposable element sequences. Nearly half of reported TCF3 translocations involve a MER20 DNA transposon. Based on this observation, we propose this sequence is important for the oncogenesis of TCF3-PBX1 acute lymphoblastic leukemia.

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