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Identification of several potential chromatin binding sites of HOXB7 and its downstream target genes in breast cancer

ABSTRACT: We report the chromatin binding sites of HOXB7 transcription factor in BT-474 breast cancer cell line using ChIP-sequencing. We validated the chromatin binding sites in BT-474, MDA-MB-361, MCF7 and T-47D breast cancer cell lines using ChIP-qPCR. The ChIP experiments have been performed using HOXB7 antibody and IgG non-specific antibody as a negative control. The direct downstream target genes of HOXB7 were identified by analyzing the expression of genes located nearby HOXB7 binding sites in HOXB7 knockdown versus control cells using qRT-PCR.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47164 | GEO | 2015/06/08

SECONDARY ACCESSION(S): PRJNA204940

REPOSITORIES: GEO

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Identification of several potential chromatin binding sites of HOXB7 and its downstream target genes in breast cancer

Project description:We report the chromatin binding sites of HOXB7 transcription factor in BT-474 breast cancer cell line using ChIP-sequencing. We validated the chromatin binding sites in BT-474, MDA-MB-361, MCF7 and T-47D breast cancer cell lines using ChIP-qPCR. The ChIP experiments have been performed using HOXB7 antibody and IgG non-specific antibody as a negative control. The direct downstream target genes of HOXB7 were identified by analyzing the expression of genes located nearby HOXB7 binding sites in HOXB7 knockdown versus control cells using qRT-PCR. Examination of chromatin binding sites of HOXB7 in BT-474 breast cancer cell line using ChIP-seq. Four parallel IgG samples were sequenced, merged together and used as a control data set. Two parallel HOXB7 ChIP samples were sequenced and merged for each replicate, AF1 and AF2. Both HOXB7 ChIP replicates (AF1 and AF2) contained approximately the same amount of reads as the merged IgG control data set.

2015-06-08 | E-GEOD-47164 | biostudies-arrayexpress

RNA-sequencing of tamoxifen-resistant and -sensitive breast cancer cell lines.

Project description:We performed RNA-sequencing on 7 tamoxifen-resistant (MCF-7 Tam1, T-47D Tam1, T-47D Tam2, ZR-75-1 Tam1, ZR-75-1 Tam2, BT474 Tam1 and BT-474 Tam2) and their isogenic parental (MCF-7, T-47D, ZR-75-1 and BT-474) breast cancer cell lines. The tamoxifen-resistant cell lines were generated from the parentel cell lines by continuous administration of 1 µM 4-OH-tamoxifen for eight to twelve months. RNA- sequencing was performed to determine the changes in the expression of genes in the resistant clones as well as pathways. In addition, we compared the expression changes of the cell lines with those of the GSE58708 data set which we reanalyzied in our pipeline.

2018-08-30 | GSE111151 | GEO

ERRalpha mediates metabolic adaptations that drive lapatinib resistance in breast cancer (ERRalpha binding profiles in breast cancer cells by ChIP-seq)

Project description:Ablation of ERRalpha significantly delays ERBB2-induced mammary tumorigenesis and ERRalpha regulates genes of the ERBB2 amplicon. To further investigate the relationship between ERRalpha activity and RTK signaling, we mapped ERRalpha binding sites in SKBr3 cells upon EGF treatment or heregulin treatment. Inhibition of ERBB2 signaling using the RTK inhibitor lapatinib impacts on ERRalpha stability, while cells resistant to lapatinib treatment exhibit restored ERRalpha expression. We therefore mapped ERRalpha binding sites in parental (sensitive) cells (pSKBr3) as well as in lapatinib-resistant cells (LRSKBr3). ChIP-Seq analysis of ERRalpha binding profile in SKBr3 or BT-474 breast cancer cells.

2016-06-15 | E-GEOD-81651 | biostudies-arrayexpress

Identification of mRNAs modulated by the HOXB7-MEK signaling cascade

Project description:Transcripts upregulated or downregulated by HOXB7-MEK signaling were identified for use on the microarray using the Affymetrix GeneChip WT PLUS Reagent Kit in comparison with HOXB7-knockdown S2-013 cells that were transfected with rescue-HOXB7 plasmid and treated with MEK inhibitor, and HOXB7-knockdown S2-013 cells that were transfected with rescue-HOXB7 plasmid but not treated with MEK inhibitor.

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Transcription profiling by array of human breast cancer cell line BT-474 with annexin A1 over-expression or silenced with siRNA to demonstrate design of multi-condition experiments

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HOXB7 is an ERα cofactor in the activation of HER2 and multiple ER target genes leading to endocrine resistance

Project description:Why breast cancers become resistant to tamoxifen despite continued expression of the estrogen receptor alpha (ERα) and what factors are responsible for high HER2 expression in these tumors remains an enigma. HOXB7 ChIP analysis followed by validation showed that HOXB7 physically interacts with ERα, and that the HOXB7-ERα complex enhances transcription of many ERα target genes including HER2. Investigating strategies for controlling HOXB7, our studies revealed that MYC, stabilized via phosphorylation mediated by EGFR-HER2 signaling, inhibits transcription of miRNA-196a, a HOXB7 repressor. This leads to increased expression of HOXB7, ER-target genes and HER2. Repressing MYC using small molecule inhibitors reverses these events, and causes regression of breast cancer xenografts. The MYC-HOXB7-HER2 signaling pathway is eminently targetable in endocrine-resistant breast cancer.

2014-11-25 | GSE63607 | GEO

HOXB7 is an ERÎ± cofactor in the activation of HER2 and multiple ER target genes leading to endocrine resistance

Project description:Why breast cancers become resistant to tamoxifen despite continued expression of the estrogen receptor alpha (ERÎ±) and what factors are responsible for high HER2 expression in these tumors remains an enigma. HOXB7 ChIP analysis followed by validation showed that HOXB7 physically interacts with ERÎ±, and that the HOXB7-ERÎ± complex enhances transcription of many ERÎ± target genes including HER2. Investigating strategies for controlling HOXB7, our studies revealed that MYC, stabilized via phosphorylation mediated by EGFR-HER2 signaling, inhibits transcription of miRNA-196a, a HOXB7 repressor. This leads to increased expression of HOXB7, ER-target genes and HER2. Repressing MYC using small molecule inhibitors reverses these events, and causes regression of breast cancer xenografts. The MYC-HOXB7-HER2 signaling pathway is eminently targetable in endocrine-resistant breast cancer. MCF7 cell lines stably transduced with either vector control of HOXB7. Array ran in duplicates.

2014-11-25 | E-GEOD-63607 | biostudies-arrayexpress

human HCC cell MHCCLM3: HOXB7-siRNA transfected vs. control

Project description:We found that HOXB7 promotes HCC cell proliferation, migration, and invasion. To further explore the mechanism, we performed a cDNA microarray assay to compare the differential gene expression profiles of HOXB7 depletion (HOXB7-siRNA-treated) and negative control siRNA-treated in MHCCLM3 cells.

2019-04-02 | GSE80104 | GEO

microRNA profiling of luminal and TNBC breast cancer cell lines

Project description:two luminal cell lines were added, MCF7 and BT-474 two TNBC cell line were added, MB231 and BT-549

2014-10-03 | GSE62022 | GEO

RNA-seq of breast cancer cell lines post ligand treatment I

Project description:Goal: study the impact of estrogen receptor ligands on gene expression in HR+ breast cancer cells Methods: RNA sequencing Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), promotes transcriptional activation of ER and mimics the transcriptional effect of natural ligand E2 for a subset of ER target genes, consistently across the seven breast cell lines (MCF-7, HCC1500, MDA-MB-330, EFM-19, T-47D, BT-474, and CAMA-1). Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand do not induce, or induce very weakly the expression of ER target genes. The effect of GDC-0810 depends on the cellular context.

2019-07-25 | GSE117942 | GEO

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