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RNA-seq of T-47D cells treated with 17-beta-estradiol and/or APOBEC3B-targeting siRNA

ABSTRACT: Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3B, A3B) is a key molecular driver inducing mutations in multiple human cancer. A3B belongs to the APOBEC3 enzyme family, which consists seven closely related DNA deaminases that catalyse cytosine-to-uracil (C>U) editing of single-stranded DNA (ssDNA). Here, we used RNA-seq technology to study the effect of A3B knockdown on the effect of estradiol induction in T-47D cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193231 | GEO | 2025/01/06

REPOSITORIES: GEO

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Whole genome sequencing of T-47D cell colonies overexpressed with APOBEC3B and hUGI

Project description:Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3B, A3B) is a key molecular driver inducing mutations in multiple human cancer. A3B belongs to the APOBEC3 enzyme family, which consists seven closely related DNA deaminases that catalyse cytosine-to-uracil (C>U) editing of single-stranded DNA (ssDNA). Here, we used a lentiviral inducible system to overexpress A3B and hUGI in T-47D cells. This system will allow augmented genomic editing by A3B, while preserving the C>U editing sites from DNA repair by inhibiting base excision repair mechanism.

2025-01-06 | GSE193226 | GEO

Strand-specific DNA:RNA immunoprecipitation sequencing on T-47D breast cancer cells.

Project description:Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3B) is a key molecular driver inducing mutations in multiple human cancer. A3B is a member of the APOBEC3 enzyme family, which consists seven closely related DNA deaminases that catalyse cytosine-to-uracil (C>U) editing of single-stranded DNA (ssDNA). Using a cell model that lacks base excision repair function, we sampled A3B editing sites in bulk. Analyses conducted on these A3B editing sites point to a function of A3B in editing DNA:RNA hybrid structure known as R-loops. In order to verify this result, we conducted strand-specific DNA:RNA immunoprecipitation sequencing (ssDRIP-seq; S9.6, KeraFAST, ENH001) on T-47D breast cancer cells.

2025-01-06 | GSE193225 | GEO

Quantified strand-specific DNA:RNA immunoprecipitation sequencing on T-47D breast cancer cells.

Project description:Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3B) is a key molecular driver inducing mutations in multiple human cancer. A3B belongs to the APOBEC3 enzyme family, which consists seven closely related DNA deaminases that catalyse cytosine-to-uracil (C>U) editing of single-stranded DNA (ssDNA). Using a cell model that lacks base excision repair function, we sampled A3B editing sites in bulk. Analyses conducted on these A3B editing sites point to a function of A3B in editing DNA:RNA hybrid structure known as R-loops. In order to verify this result, we conducted strand-specific DNA:RNA immunoprecipitation sequencing (ssDRIP-seq; S9.6, KeraFAST, ENH001) on T-47D breast cancer cells.

2025-01-06 | GSE193229 | GEO

ChIP-seq of TDRD3, CARM1 and H3R17me2a in T-47D cells

Project description:Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3B, A3B) is a key molecular driver inducing mutations in multiple human cancer. A3B belongs to the APOBEC3 enzyme family, which consists seven closely related DNA deaminases that catalyse cytosine-to-uracil (C>U) editing of single-stranded DNA (ssDNA). By using mass-spec proteomics, we identified TDRD3, a ‘reader’ of asymmetrically methylated arginine marks, as the binding partner of A3B.

2025-01-06 | GSE193232 | GEO

Mapping and quantification of single-strand DNA bound by flag-tagged APOBEC3B

Project description:Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3B, A3B) is a key molecular driver inducing mutations in multiple human cancer. A3B belongs to the APOBEC3 enzyme family, which consists seven closely related DNA deaminases that catalyse cytosine-to-uracil (C>U) editing of single-stranded DNA (ssDNA). Here, we adopted single-strand DNA protein-immunoprecipitation sequencing (SPI-seq) to capture the ssDNA bound by flag-tagged A3B protein. Quantification on sequence reads was carried out to investigate the effect of 17-beta estradiol (E2) on A3B binding to DNA.

2025-01-06 | GSE193228 | GEO

Detection of DNA double-strand breaks in T-47D cells using DSBCapture-seq

Project description:Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3B, A3B) is a key molecular driver inducing mutations in multiple human cancer. A3B belongs to the APOBEC3 enzyme family, which consists seven closely related DNA deaminases that catalyse cytosine-to-uracil (C>U) editing of single-stranded DNA (ssDNA). Here, we used DSBCapture-seq to study the formation of DNA double-strand breaks (DSB) by estrogen receptor activation upon 17-estradiol (E2) induction. The effect of A3B-depletion on DSB formation was investigated using RNA interference.

2025-01-06 | GSE193230 | GEO

Mapping the genomic occupancy by flag-tagged APOBEC3B protein

Project description:Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3B) is a key molecular driver inducing mutations in multiple human cancers. APOBEC3B belongs to the APOBEC3 enzyme family, which consists seven closely related DNA deaminases that catalyse cytosine-to-uracil (C>U) editing of single-stranded DNA (ssDNA). In order to investigate the genomic binding sites of APOBEC3B, high through-put sequencing experiments were conducted using DNA samples acquired by standard chromatin immunoprecipitation (ChIP) and ssDNA protein immunoprecipitation (SPI) samples. Substrate preference by APOBEC3B were characterised by comparing these results.

2025-01-06 | GSE193227 | GEO

Detection of APOBEC3B-mediated RNA editing sites in T-47D cells [RNA-seq]

Project description:RNA editing is a crucial post-transcriptional process that diversifies proteomic outcomes and influences gene expression. Particularly, the APOBEC3 family has emerged as a significant player in this mechanism, with APOBEC3A (A3A) showing notable roles in immune response and stress conditions. APOBEC3B (A3B), another family member, has garnered attention for its potential role in breast cancer genomic mutations. In this study, we employ an inducible expression cell model and a novel methodology for identifying differential variants in RNA (DVRs) to map A3B-mediated RNA editing sites in a breast cancer cell model. Our findings indicate that A3B engages in selective RNA editing and targets NEAT1 and MALAT1 long non-coding RNAs. Notably, the binding of these RNAs sequesters A3B’s catalytic activity, and thereby affects A3A’s activity through a feedback loop.

2024-08-14 | GSE245700 | GEO

Detection of APOBEC3B's RNA binding sites in T-47D cells using eCLIP-seq

Project description:RNA editing is a crucial post-transcriptional process that diversifies proteomic outcomes and influences gene expression. Particularly, the APOBEC3 family has emerged as a significant player in this mechanism, with APOBEC3A (A3A) showing notable roles in immune response and stress conditions. APOBEC3B (A3B), another family member, has garnered attention for its potential role in breast cancer genomic mutations. In this study, we employ an inducible expression cell model and eCLIP-seq to detect the RNA binding sites for A3B a breast cancer cell model. Our findings indicate that A3B engages in selective RNA editing and targets NEAT1 and MALAT1 long non-coding RNAs. Notably, the binding of these RNAs sequesters A3B’s catalytic activity, and thereby affects A3A’s activity through a feedback loop.

2024-08-14 | GSE245701 | GEO

APOBEC3B facilitates a functional and necessary link between estrogen receptor mediated transcription and DNA repair

Project description:Oestrogen receptor-α (ER) is the principal transcription factor in the majority of breast cancers, driving expression of genes that control cell growth and endocrine response. Understanding the mechanisms of ER action is crucial for improving response to endocrine treatments. Recent studies show that cytosine deaminase (CD) activity is an important source of cancer mutations. In particular, APOBEC3B (A3B) promotes mutagenesis in breast cancer cells1. Our analysis of breast cancer expression datasets showed that A3B expression predicts for poor survival in ER-positive, but not in ER-negative patients, indicative of a link with ER activity. Chromatin immunoprecipitation coupled to deep sequencing (ChIP-seq) used to map global A3B binding sites showed a remarkable oestrogen-stimulated recruitment of A3B to ER binding sites. Functionally, A3B was critical for ER transcriptional activity and regulated breast cancer cell proliferation. We show that A3B regulates ER transcription by promoting cytosine deamination and activation of DNA strand break repair at ER binding regions. We propose that cytosine deamination and DNA strand break generation by A3B facilitates gene expression by aiding chromatin remodeling at ER target genes. Our findings also suggest a mechanism by which subversion of transcription factor mediated recruitment of cytosine deaminases promotes cancer mutations. Hormone-depleted MCF-7 breast cancer cell line was treated with estrogen (100 nM), H2O2 (10 mM) or vehicle for 45 minutes. H2AX ChIP-seq was performed using Illumina methodology.

2015-09-07 | E-GEOD-57426 | biostudies-arrayexpress

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