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EGFR-induced lncRNA TRIDENT promotes drug resistance in non–small cell lung cancer via phospho-TRIM28-mediated DNA damage repair

ABSTRACT: EGFR-induced lncRNA TRIDENT promotes drug resistance in non–small cell lung cancer via phospho-TRIM28-mediated DNA damage repair

PROVIDER: PRJNA1220160 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32259400_1.fastq.gz	Fastqsanger.gz
	SRR32259400_2.fastq.gz	Fastqsanger.gz
	SRR32259401_1.fastq.gz	Fastqsanger.gz
	SRR32259401_2.fastq.gz	Fastqsanger.gz
	SRR32259366_1.fastq.gz	Fastqsanger.gz

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EGFR-induced lncRNA TRIDENT promotes drug resistance in non–small cell lung cancer via phospho-TRIM28-mediated DNA damage repair

Project description:Long noncoding RNAs (lncRNAs) play numerous roles in cellular biology and alterations in lncRNA expression profiles have been implicated in a variety of cancers. Here, we identify and characterize a n lncRNA, TRIM28 Interacting DNA damage repair Enhancing Noncoding Transcript (TRIDENT), whose expression is induced upon epithelial growth factor receptor (EGFR) activation, and which exerts pro-oncogenic functions in EGFR-driven non–small cell lung cancer. Knocking down TRIDENT leads to decreased tumor-cell proliferation in both in vitro and in vivo model systems and induces sensitization to chemotherapeutic drugs. Using ChIRP-MS analysis we identified TRIM28 as a protein interactor of TRIDENT. TRIDENT promotes phosphorylation of TRIM28 and knocking down TRIDENT leads to accumulation of DNA damage in cancer cells via decreased TRIM28 phosphorylation. Altogether, our results reveal a molecular pathway in which TRIDENT regulates TRIM28 phosphorylation to promote tumor cell growth and drug resistance. Our findings suggest that TRIDENT can be developed as a biomarker or therapeutic target for EGFR mutant non–small cell lung cancer.

2025-02-06 | GSE288985 | GEO

Effect of DNA damage on ligand stimulated EGFR signaling pathways

Project description:We examined the cellular response of primary normal cells to EGFR stimulation under normal and DNA damage conditions.

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Mouse models with defective DNA damage repair

Project description:Mouse models with defective DNA damage repair

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CPD-seq mapping of UV damage formation and repair in yeast

Project description:UV-induced DNA lesions are an important contributor to mutagenesis and cancer, but it is not fully understood how the chromosomal landscape influences UV lesion formation and repair. We have used a novel high-throughput sequencing method to precisely map UV-induced cyclobutane pyrimidine dimers (CPDs) at nucleotide resolution throughout the yeast genome. Analysis of CPD formation reveals that nucleosomal DNA having an inward rotational setting is protected from CPD lesions. In strongly positioned nucleosomes, this nucleosome 'photofootprint' overrides intrinsic dipyrimidine sequence preferences for CPD formation. CPD formation is also inhibited by DNA-bound transcription factors, in effect protecting important DNA elements from UV damage. Analysis of CPD repair revealed a clear signature of efficient transcription-coupled nucleotide excision repair. Repair was less efficient at translational positions near a nucleosome dyad and at heterochromatic regions in the yeast genome. These findings define the roles of nucleosomes and transcription factors in UV damage formation and repair. UV mapping data was analyzed for yeast cells irradiated with 125J/m2 and allowed to repair for 0hr (2 samples), 20 minutes, 1 hour, or 2 hours. Data is also included for naked DNA irradiated with UV 60 or 90 J/m2

2016-08-19 | E-GEOD-79977 | biostudies-arrayexpress

The role of KDM6B in DNA damage repair

Project description:The role of KDM6B in DNA damage repair

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Excision repair hotspots of UV-induced DNA damage in the human genome

Project description:We recently developed high-throughput sequencing approaches, eXcision Repair sequencing (XR-seq) and Damage-seq, to generate genome-wide mapping of DNA damage formation and excision repair, respectively, with single-nucleotide resolution. Here, we adopted time-course XR-seq data to profile UV-induced excision repair dynamics, paired with Damage-seq data to quantify the overall induced DNA damage. We identified genome-wide repair hotspots that are subject to exemplified amount of repair very soon after UV irradiation. We show that such repair hotspots do not result from hypersensitivity to DNA damage and are thus not damage hotspots. We find that the earliest repair occur preferentially in promoters and enhancers from open-chromatin regions. The repair hotspots are also significantly enriched for frequently interacting regions and super-enhancers, both of which are hotspots for local chromatin interactions. We further extend the interrogation of chromatin organization to DNA replication timing and conclude that early-repair hotspots are enriched for early-replication domains. Collectively, we report genome-wide early-repair hotspots of UV-induced damage, in association with chromatin states and epigenetic compartmentalization of the human genome.

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Silencing of TRIM28 in human iPSC

Project description:TRIM28, a multi-domain protein, is crucial in the development of mouse embryos and the maintenance of embryonic stem cells (ESC) self-renewal potential. As the epigenetic factor modulating the structure of chromatin, TRIM28 regulates the expression of numerous genes and is associated with progression and poor prognosis in many types of cancer. IPSC served as a model of the cells with stem cell-like phenotype, e.g., cancer stem cells. We evaluated the role of TRIM28 in pluripotency maintenance in iPSC by silencing endogenous TRIM28 expression with siRNA (iPSC-siTRIM28). IPSC treated with siRNA with no target sequence served as a control (siCTRL) of the experiment. Cells lacking TRIM28 lose the expression of pluripotency markers, as well as the ability to self-renew, and they start to differentiate. Pathway enrichment analysis using Gene Ontology datasets showed significant upregulation of pathways related to apoptosis, differentiation, cellular response to DNA damage stimulus and cell cycle regulation in iPSC-siTRIM28, relative to reference iPSC (iPSC-WT and iPSC-siCTRL).

2020-07-03 | GSE153726 | GEO

Dynamic Maps of UV Damage Formation and Repair for the Human Genome

Project description:UV-induced DNA damage is the major carcinogen of skin cancer. We developed HS-Damage-seq to map UV damage with unprecedented sensitivity and resolution in human cells. While the distribution of UV-induced damage are mainly determined by sequence context and essentially uniform throughout the genome, transcription factors can affect damage formation at specific positions. With time-course experiments, we observed changes in damage distribution at particular genomic loci and chromatin states, which reflects the nucleotide excision repair preferences and complements the repair maps by XR-seq. Our results demonstrated that while initial damage is uniformly distributed, they are heterogeneously repaired throughout the genome. The combination of damage and repair maps provides a holistic perspective of UV damage and repair in the human genome.

2017-06-27 | GSE98025 | GEO

Novel antibody-peptide binding assay indicates presence of immunoglobulins against EGFR phospho-site S1166 in high-grade glioma.

Project description:The project’s aim was to develop and test the applicability of a method to determine the presence of serum immunoglobulins against specific autoantibodies. The method combined immunoglobulin G enrichment (using Melon Gel), molecular weight filtration, and targeted mass spectrometry and the feasibility was successfully tested in an experiment using a peptide library (tryptic digest) of dinitrophenyl labelled peptides and anti-DNP. In a second step, a phospho-peptide library, derived from glioblastoma multiform tissue, was tested against plasma samples from glioma patients and healthy donors, to determine the presence of complexes of IgG with immunoaffinity to EGFR or GFAP phospho-peptides. As a result, we found immunoaffinity to EGFR phospho-peptide GSHQIS[+80]LDNPDYQQDFFPK (covering the phospho-site S1166) in plasma of glioma patients.

2022-06-09 | PXD032844 | Pride

Effect of DNA damage on ligand stimulated EGFR signaling pathways

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