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The ETS transcription factor Elf5 drives lung metastasis in luminal breast cancer via recruitment of Gr-1+CD11b+ myeloid derived suppressor cells

ABSTRACT: The ETS transcription factor Elf5 drives lung metastasis in luminal breast cancer via recruitment of Gr-1+CD11b+ myeloid derived suppressor cells

PROVIDER: PRJNA253292 | ENA |

REPOSITORIES: ENA

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The ETS transcription factor Elf5 drives lung metastasis in luminal breast cancer via recruitment of Gr-1+CD11b+ myeloid derived suppressor cells [acute]

Project description:Elf5 expression in mammary progenitor cells regulates a cell fate decision that establishes the alveolar cell lineage. In luminal breast cancer cells, increased Elf5 expression suppressed estrogen receptor and FoxA1 expression and was implicated in the acquisition of resistance to the cytostatic effects of antiestrogen therapy. We show that in the PyMT model of luminal breast cancer, increased Elf5 expression drives lung metastasis by recruiting myeloid-‐derived suppressor cells, and that this activity overcomes the epithelializing influence of Elf5. Breast cancer expression signatures identify a similar process in humans, and increased Elf5 immunohistochemical staining predicts poor prognosis in the luminal A subgroup. Thus Elf5 may promote escape from hormonal therapy and drive metastasis in luminal breast cancer.

2015-12-30 | GSE58726 | GEO

The ETS transcription factor Elf5 drives lung metastasis in luminal breast cancer via recruitment of Gr-1+CD11b+ myeloid derived suppressor cells [chronic]

2015-12-30 | GSE58728 | GEO

The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [human]

Project description:The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. Elf5 was knocked down via siRNA in basal HCC1937 cell lines, in triplicate. Elf5 was induced in luminal T47D and MCF7 cell lines via a doxycycline inducible expression vector, in duplicate.

2012-12-27 | E-GEOD-30405 | biostudies-arrayexpress

The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [mouse]

Project description:The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. Elf5 was induced via doxycycline treated PyMT mouse tumours, in triplicate

2014-01-13 | E-GEOD-30406 | biostudies-arrayexpress

The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [human]

2012-12-27 | GSE30405 | GEO

The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [mouse]

2014-01-13 | GSE30406 | GEO

The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [human ChIP-Seq]

Project description:The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. ChIP-Seq using an antibody to ELF5, in T47D breast carcinoma cell lines

2012-12-27 | E-GEOD-31216 | biostudies-arrayexpress

ETS transcription factor ELF5 modulates estrogen action in breast cancer via participation in FOXA1-ER driven transcription

2020-05-26 | PXD013349 | Pride

The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [human ChIP-Seq]

2012-12-27 | GSE31216 | GEO

The ETS transcription factor ELF5 modulates estrogen action in breast cancer via participation in FOXA1-ER driven transcription.

Project description:The ETS transcription factor ELF5 drives mammary alveolar development in preparation for lactation by forcing differentiation within the progenitor cell population. In luminal A breast cancer, early disease progression is predicted by high levels of ELF5, and in preclinical models elevated ELF5 is associated with its two key features, the acquisition of resistance to endocrine therapy and increased metastasis. We first created an MCF7 cell line with doxycycline-inducible ELF5 and then examined with ChIP-seq differences in genomic binding of FOXA1, ER and H3K4me3 upon doxycycline treatment, compared to vehicle. In addition we performed RNA-seq experiments to examine changes in gene expression upon induction of ELF5 expression. Here we demonstrate that ELF5 binding overlaps with FOXA1 and ER at enhancers and promoters, and when elevated causes FOXA1 and ER to bind to new regions of the genome involved in resistance to endocrine therapy. RNA-seq demonstrated that these changes altered gene expression to diminish estrogen influence, and that ELF5 regulated the expression of ER transcription-complex genes. These data show that ELF5 modulated estrogen-driven transcription in breast cancer by directing FOXA1 and ER to new genomic locations, and by interaction with, and regulation of, members of the ER transcriptional complex. This provides a mechanistic basis for the influence of ELF5 on the progression of luminal breast cancer to endocrine insensitivity.

2020-01-06 | E-MTAB-7641 | biostudies-arrayexpress

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