Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA357727 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression analysis on MEL-18-knockdown BT474 cells. MEL-18, a polycomb group protein and a member of the polycomb repressive complex 1 (PRC1), have suggested as a tumor suppressor in several cancer, including breast cancer. The results provides that the depletion of MEL-18 in HER2-positive breast cancer causes the activation of ErbB signaling pathway. We proposed that MEL-18 is a novel prognostic and therapeutic marker for HER2-positive breast cancer.
2018-07-31 | GSE92504 | GEO
Project description:RNA-sequencing analysis of MEL-18 WT- or MEL-18 T334A-overexpressing MDA-MB-231 cell lines. MEL-18, a core component of polycomb-repressive complex (PRC)-1, has been known to be phosphorylated at multiple residues in vitro; however, its functional roles in mammalian cells and human cancer remains largely unknown. Here, we examined the effect of MEL-18 phosphorylation at T334 site on polycomb-mediated epigenetic silencing in human breast cancer. Our results demonstrated that the phosphorylation of MEL-18 at T334 alters its genomic distribution and transcriptional activity that reflects functional change of MEL-18 in modulating breast tumour progression.
2022-03-01 | GSE115591 | GEO
Project description:ChIP-seq analysis of MEL-18 WT- or MEL-18 T334A-overexpressing MDA-MB-231 cell lines. MEL-18, a core component of polycomb-repressive complex (PRC)-1, has been known to be phosphorylated at multiple residues in vitro; however, its functional roles in mammalian cells and human cancer remains largely unknown. Here, we examined the effect of MEL-18 phosphorylation at T334 site on polycomb-mediated epigenetic silencing in human breast cancer. Our results demonstrated that the phosphorylation of MEL-18 at T334 alters its genomic distribution and transcriptional activity that reflects functional change of MEL-18 in modulating breast tumour progression.
2022-03-01 | GSE115586 | GEO
Project description:Gene expression analysis of MEL-18-silenced MCF7 cell lines. MEL-18 is a component of the polycomb repressive complex (PRC)-1, which is a critical epigenetic modulator of stem cell regulation and normal and cancerous development. Accumulating studies have suggested that MEL-18 might act as a tumor suppressor in several human tumors, including breast cancer. Results provide insight into the functional role of MEL-18 in estrogen-dependent breast cancer.
2015-05-01 | GSE64716 | GEO
Project description:Gene expression analysis of MEL-18-silenced MCF7 cell lines. MEL-18 is a component of the polycomb repressive complex (PRC)-1, which is a critical epigenetic modulator of stem cell regulation and normal and cancerous development. Accumulating studies have suggested that MEL-18 might act as a tumor suppressor in several human tumors, including breast cancer. Results provide insight into the functional role of MEL-18 in estrogen-dependent breast cancer. MCF7 cells stably infected with lentiviruses encoding either control (shCon) or MEL-18 shRNA (shMEL) were cultured in phenol-red free DMEM supplemented with 10% FBS for 48 h. Total RNA was isolated from the cultures using Trizol reagent. For each of the 2 conditions, 2 biological replicates were included. In total, 4 microarray samples were analyzed; 2 controls and 2 shRNA MEL-18 knockdowns. All labeling, hybridization and scanning steps were performed according to the manufacturers’ instructions.
2015-05-01 | E-GEOD-64716 | biostudies-arrayexpress
Project description:Forkhead box protein A1 (FOXA1) has been shown to have critical functions in prostate and ER alpha positive breast cancer. As a pioneering transcriptional factor, FOXA1 regulates DNA accessibility for the androgen receptor in prostate and the estrogen receptor alpha in ER positive breast cancer, respectively. FOXA1 is also expressed in human epidermal growth factor receptor-2 (HER2/ErbB2) positive breast cancers, but its functions in HER2 positive breast cancer are unclear. The loss of FOXA1 results in a decrease in the viability of HER2 positive and HER2 amplified cell lines suggesting that FOXA1 may have an important role in HER2 positive breast cancers. In this report, we examined patient-derived single-cell RNA sequencing and spatial transcriptomics data and demonstrated that FOXA1 is co-expressed with ErbB2 in HER2 positive breast cancers. Knocking down FOXA1 expression led to the reduction of HER2 expression and signaling. Chromatin Immunoprecipitation Sequencing (ChIP-seq) and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) identified FOXA1 binding motifs in the ErbB2 promoter and regulatory element regions, which controlled ErbB2 gene expression. Interestingly, the knockdown of FOXA1 increased Epithelial Mesenchymal Transition (EMT) signaling and inhibited luminal tumor differentiation. Furthermore, FOXA1 and TRPS1 regulated TEAD/YAP-TAZ activity. Taken together, our data demonstrate that FOXA1 is required for HER2 expression and luminal identity in HER2+ breast cancer.
2024-09-01 | GSE267920 | GEO
Project description:Forkhead box protein A1 (FOXA1) has been shown to have critical functions in prostate and ER alpha positive breast cancer. As a pioneering transcriptional factor, FOXA1 regulates DNA accessibility for the androgen receptor in prostate and the estrogen receptor alpha in ER positive breast cancer, respectively. FOXA1 is also expressed in human epidermal growth factor receptor-2 (HER2/ErbB2) positive breast cancers, but its functions in HER2 positive breast cancer are unclear. The loss of FOXA1 results in a decrease in the viability of HER2 positive and HER2 amplified cell lines suggesting that FOXA1 may have an important role in HER2 positive breast cancers. In this report, we examined patient-derived single-cell RNA sequencing and spatial transcriptomics data and demonstrated that FOXA1 is co-expressed with ErbB2 in HER2 positive breast cancers. Knocking down FOXA1 expression led to the reduction of HER2 expression and signaling. Chromatin Immunoprecipitation Sequencing (ChIP-seq) and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) identified FOXA1 binding motifs in the ErbB2 promoter and regulatory element regions, which controlled ErbB2 gene expression. Interestingly, the knockdown of FOXA1 increased Epithelial Mesenchymal Transition (EMT) signaling and inhibited luminal tumor differentiation. Furthermore, FOXA1 and TRPS1 regulated TEAD/YAP-TAZ activity. Taken together, our data demonstrate that FOXA1 is required for HER2 expression and luminal identity in HER2+ breast cancer.
2024-09-01 | GSE267921 | GEO
Project description:Forkhead box protein A1 (FOXA1) has been shown to have critical functions in prostate and ER alpha positive breast cancer. As a pioneering transcriptional factor, FOXA1 regulates DNA accessibility for the androgen receptor in prostate and the estrogen receptor alpha in ER positive breast cancer, respectively. FOXA1 is also expressed in human epidermal growth factor receptor-2 (HER2/ErbB2) positive breast cancers, but its functions in HER2 positive breast cancer are unclear. The loss of FOXA1 results in a decrease in the viability of HER2 positive and HER2 amplified cell lines suggesting that FOXA1 may have an important role in HER2 positive breast cancers. In this report, we examined patient-derived single-cell RNA sequencing and spatial transcriptomics data and demonstrated that FOXA1 is co-expressed with ErbB2 in HER2 positive breast cancers. Knocking down FOXA1 expression led to the reduction of HER2 expression and signaling. Chromatin Immunoprecipitation Sequencing (ChIP-seq) and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) identified FOXA1 binding motifs in the ErbB2 promoter and regulatory element regions, which controlled ErbB2 gene expression. Interestingly, the knockdown of FOXA1 increased Epithelial Mesenchymal Transition (EMT) signaling and inhibited luminal tumor differentiation. Furthermore, FOXA1 and TRPS1 regulated TEAD/YAP-TAZ activity. Taken together, our data demonstrate that FOXA1 is required for HER2 expression and luminal identity in HER2+ breast cancer.
2024-09-01 | GSE267919 | GEO
Project description:DCD is a gene amplified and overexpressed in a subset of breast tumors acting as a growth and survival factor. Patients with DCD-positive breast cancer have worse prognostic features. To investigate the role of DCD in breast tumorigenesis, we analyzed the consequences of its downregulation in human breast cancer cell lines using three specific shRNA lentivirus vectors. Genes up- and down-regulated by DCD were identified using Affymetrix microarray and analyzed by MetaCore Platform. We found that loss of DCD expression led to reduced cell proliferation, resistance to apoptosis, and suppressed tumorigenesis in immunodeficient mice. Network analysis of gene expression data revealed perturbed ERBB signaling following DCD shRNA expression including changes in the expression of ERBB receptors and their ligands. These findings imply that DCD promotes breast tumorigenesis via modulating the activity of the ERBB signaling pathways. As ERBB signaling is also important for neural survival, HER2+ breast tumors may highjack DCD’s neural survival-promoting functions to promote tumorigenesis.
2015-08-12 | GSE57578 | GEO
Project description:A total of 79 breast tumors (71 malignant tumors, 6 fibroadenomas, and 2 DCIS) were studied and compared to the reduction mammoplastic specimens of 12 healthy women as well as adjacent cancer-free tissue for 23 of the malignant tumors. Polycomb Group (PcG) proteins Bmi-1 and Mel-18 were then studied more closely first on mRNA expression level using microarray data from two of our ongoing projects and then on protein expression level using immunohistochemistry.
2010-07-01 | E-MTAB-271 | biostudies-arrayexpress