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Transcript-specific differences in m6A modifications in endocrine-sensitive and resistant breast cancer cells

ABSTRACT: Transcript-specific differences in m6A modifications in endocrine-sensitive and resistant breast cancer cells

PROVIDER: PRJNA1114102 | ENA |

REPOSITORIES: ENA

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Transcript-specific differences in m6A modifications in endocrine-sensitive and resistant breast cancer cells II

Project description:Transcript-specific differences in m6A modifications in endocrine-sensitive and resistant breast cancer cells II

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Transcript-specific differences in m6A modifications in endocrine-sensitive and resistant breast cancer cells

Project description:Acquired resistance to endocrine therapies (ET) remains a clinical problem for breast cancer patients whose initial tumors express estrogen receptor α (ER). Epigenetic changes are among the mechanisms involved in the development of ET resistance. We tested the hypothesis that the epitranscriptomic modification N-6 methyladenosine (m6A) differentially regulates the abundance of mRNA transcripts in ET-sensitive MCF-7 versus LCC9 ET-resistant ER+ human breast cancer cells. Direct mRNA sequencing (dRNA-seq) was performed on five replicates for each cell line +/- treatment with 100 nM 4-hydroxytamoxifen (4-OHT) using Nanopore MinION long read RNA-seq. Parallel short read Illumina RNA-seq was used to quantify differential transcript abundance. Statistical analysis integrated m6Anet, a machine-learning algorithm designed to call m6A modified bases, with a generalized linear model following a binomial distribution analysis to identify significant differential m6A modification ratios (DMR). Our findings reveal distinct m6A modification patterns in ET-resistant LCC9 breast cancer cells and in response to 4-OHT treatment compared to their ET-sensitive parental MCF-7 cells, suggesting a potential role for epitranscriptomic alterations in the development of ET resistance.

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Transcript-specific differences in m6A modifications in endocrine-sensitive and resistant breast cancer cells II

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Phosphoproteomics measurement of clonal endocrine therapy sensitive and resistant breast cancer populations

Project description:Around two thirds of breast tumors are characterized by the expression of estrogen receptor α and are therapeutically treated by blocking estrogen signaling. First line endocrine therapeutics are Tamoxifen which displaces estrogen form its receptor preventing receptor activation and aromatase inhibitors which prevent the formation of estrogen and thereby hormone-deprive the tumors. Therapy resistance remains a major clinical problem, especially for patients with late-stage diagnoses. Tumor heterogeneity may promote therapy resistance either through the selection of pre-existing rare clones or by providing a repertoire of cells that may develop resistance over time. In order to study endocrine therapy resistance on a clonal level, we have developed barcoded (allowing the tracking of single cells) endocrine therapy sensitive and resistant breast cancer cell lines. From these complex cell pools, multiple single cells characterized by a specific barcode were isolated and grown out. We then subjected the clones to phosphoproteomics measurement by Mass spectrometry. Based on their phosphorylation pattern, the kinase activity profiles of endocrine therapy resistant clones were determined to identify differentially activated kinases with implications in therapy resistance.

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HMGB2 in endocrine resistant breast cancer

Project description:HMGB2 and ER ChIPseq was investigated in the MCF-7 endocrine sensitive and LY2 endocrine resistant cell lines upon treatment with Tamoxifen.

2014-09-18 | E-MTAB-1865 | biostudies-arrayexpress

Genome-wide reprogramming of the chromatin landscape underlies endocrine therapy resistance in breast cancer

Project description:The estrogen receptor alpha (ERa) drives the growth of two-thirds of all breast cancers. Endocrine therapy impinges on estrogen-induced ERa activation to block tumor growth. However, half of ERa-positive breast cancers are tolerant or acquire endocrine therapy resistance. Here we demonstrate that breast cancer cells undergo genome-wide reprogramming of their chromatin landscape, defined by epigenomic maps and chromatin openness, as they acquire resistance to endocrine therapy. This reveals a role for the Notch pathway while excluding classical ERa signaling. In agreement, blocking Notch signaling, using gamma-secretase inhibitors, or targeting its downstream gene PBX1 abrogates growth of endocrine therapy-resistant breast cancer cells. Moreover Notch signaling through PBX1 directs a transcriptional program predictive of tumor outcome and endocrine therapy response. Comparing histone modifications (H3K4me2 and H3K36me3), chromatin openness (FAIRE) and PBX1 binding between endocrine therapy sensitive MCF7 and resistant MCF7-LTED cells.

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Project description:Genome wide anaylsis of histone modifications in rats exposed to endocrine disruptors. [ChIP-Seq]

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Genome wide anaylsis of transcriptome modifications in rats exposed to endocrine disruptors. [RNA-Seq]

Project description:Genome wide anaylsis of transcriptome modifications in rats exposed to endocrine disruptors. [RNA-Seq]

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