Estrogen Receptor Activation Time Course at 3, 6, 12 & 24h in MCF7, T47D and MDA-MB-231 with and without ZMIZ1 knockdown
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE133381 | GEO | 2021/04/27
REPOSITORIES: GEO
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Project description:Estrogen Receptor Activation Time Course at 3, 6, 12 & 24h in MCF7, T47D and MDA-MB-231 with and without ZMIZ1 knockdown
| PRJNA551294 | ENA
Project description:The endometrial expression and activity of the transcriptional co-regulator, Zinc Finger MIZ-Type Containing 1 (Zmiz1), that is co-localized with a mouse uterine estrogen receptor α (ERα)-binding super-enhancer, has not yet been evaluated. In human endometrial biopsy samples ZMIZ1 transcript and protein is dynamically expressed during the menstrual cycle. ZMIZ1 mutations are associated with some uterine tumors and ZMIZ1 RNA levels are increased in endometrium from individuals with endometriosis. Disrupting ZMIZ1 in cultured human endometrial stromal cells or in mouse uterus prevented hormone-dependent proliferation of epithelial and stromal cells as well as decidual differentiation of stroma cells, triggering sterility. Additionally, aging-dependent fibrosis was accelerated in Zmiz1-targeted mouse uterus. Notably, ZMIZ1 deletion impacted expression of stromal cell progesterone receptor (PGR), which is essential for decidual transformation. Transcriptomic analyses revealed that loss of ZMIZ1 alters the amplitude of estrogen regulated gene responses, indicating ZMIZ1 fine-tunes endometrial cell signals needed for optimal functioning. ZMIZ1 and ERα were co-localized in nuclei of mouse uterine cells. E2F, CCNA2 and FOXM1 signaling were all decreased when ZMIZ1 was targeted, which likely underlies reduced cell cycle progression. Our findings demonstrate the importance of ZMIZ1 as an ERα co-regulator in uterine biology and pathology.
2025-09-22 | GSE288806 | GEO
Project description:The endometrial expression and activity of the transcriptional co-regulator, Zinc Finger MIZ-Type Containing 1 (Zmiz1), that is co-localized with a mouse uterine estrogen receptor α (ERα)-binding super-enhancer, has not yet been evaluated. In human endometrial biopsy samples ZMIZ1 transcript and protein is dynamically expressed during the menstrual cycle. ZMIZ1 mutations are associated with some uterine tumors and ZMIZ1 RNA levels are increased in endometrium from individuals with endometriosis. Disrupting ZMIZ1 in cultured human endometrial stromal cells or in mouse uterus prevented hormone-dependent proliferation of epithelial and stromal cells as well as decidual differentiation of stroma cells, triggering sterility. Additionally, aging-dependent fibrosis was accelerated in Zmiz1-targeted mouse uterus. Notably, ZMIZ1 deletion impacted expression of stromal cell progesterone receptor (PGR), which is essential for decidual transformation. ZMIZ1 and ERα were co-localized in nuclei of mouse uterine cells, and E2F, CCNA2 and FOXM1 signaling were all decreased when ZMIZ1 was targeted, which likely underlies reduced cell cycle progression. Transcriptomic analyses revealed that loss of ZMIZ1 alters the amplitude of estrogen regulated gene responses, indicating ZMIZ1 fine-tunes endometrial cell signals needed for optimal functioning. Our findings demonstrate the importance of ZMIZ1 as an ERα co-regulator in uterine biology and pathology.
2025-09-22 | GSE288877 | GEO
Project description:The endometrial expression and activity of the transcriptional co-regulator, Zinc Finger MIZ-Type Containing 1 (Zmiz1), that is co-localized with a mouse uterine estrogen receptor α (ERα)-binding super-enhancer, has not yet been evaluated. In human endometrial biopsy samples ZMIZ1 transcript and protein is dynamically expressed during the menstrual cycle. ZMIZ1 mutations are associated with some uterine tumors and ZMIZ1 RNA levels are increased in endometrium from individuals with endometriosis. Disrupting ZMIZ1 in cultured human endometrial stromal cells or in mouse uterus prevented hormone-dependent proliferation of epithelial and stromal cells as well as decidual differentiation of stroma cells, triggering sterility. Additionally, aging-dependent fibrosis was accelerated in Zmiz1-targeted mouse uterus. Notably, ZMIZ1 deletion impacted expression of stromal cell progesterone receptor (PGR), which is essential for decidual transformation. ZMIZ1 and ERα were co-localized in nuclei of mouse uterine cells, and E2F, CCNA2 and FOXM1 signaling were all decreased when ZMIZ1 was targeted, which likely underlies reduced cell cycle progression. Transcriptomic analyses revealed that loss of ZMIZ1 alters the amplitude of estrogen regulated gene responses, indicating ZMIZ1 fine-tunes endometrial cell signals needed for optimal functioning. Our findings demonstrate the importance of ZMIZ1 as an ERα co-regulator in uterine biology and pathology.
2025-09-22 | GSE288994 | GEO
Project description:The endometrial expression and activity of the transcriptional co-regulator, Zinc Finger MIZ-Type Containing 1 (Zmiz1), that is co-localized with a mouse uterine estrogen receptor α (ERα)-binding super-enhancer, has not yet been evaluated. In human endometrial biopsy samples ZMIZ1 transcript and protein is dynamically expressed during the menstrual cycle. ZMIZ1 mutations are associated with some uterine tumors and ZMIZ1 RNA levels are increased in endometrium from individuals with endometriosis. Disrupting ZMIZ1 in cultured human endometrial stromal cells or in mouse uterus prevented hormone-dependent proliferation of epithelial and stromal cells as well as decidual differentiation of stroma cells, triggering sterility. Additionally, aging-dependent fibrosis was accelerated in Zmiz1-targeted mouse uterus. Notably, ZMIZ1 deletion impacted expression of stromal cell progesterone receptor (PGR), which is essential for decidual transformation. ZMIZ1 and ERα were co-localized in nuclei of mouse uterine cells, and E2F, CCNA2 and FOXM1 signaling were all decreased when ZMIZ1 was targeted, which likely underlies reduced cell cycle progression. Transcriptomic analyses revealed that loss of ZMIZ1 alters the amplitude of estrogen regulated gene responses, indicating ZMIZ1 fine-tunes endometrial cell signals needed for optimal functioning. Our findings demonstrate the importance of ZMIZ1 as an ERα co-regulator in uterine biology and pathology.
2025-09-22 | GSE288883 | GEO
Project description:The endometrial expression and activity of the transcriptional co-regulator, Zinc Finger MIZ-Type Containing 1 (Zmiz1), that is co-localized with a mouse uterine estrogen receptor α (ERα)-binding super-enhancer, has not yet been evaluated. In human endometrial biopsy samples ZMIZ1 transcript and protein is dynamically expressed during the menstrual cycle. ZMIZ1 mutations are associated with some uterine tumors and ZMIZ1 RNA levels are increased in endometrium from individuals with endometriosis. Disrupting ZMIZ1 in cultured human endometrial stromal cells or in mouse uterus prevented hormone-dependent proliferation of epithelial and stromal cells as well as decidual differentiation of stroma cells, triggering sterility. Additionally, aging-dependent fibrosis was accelerated in Zmiz1-targeted mouse uterus. Notably, ZMIZ1 deletion impacted expression of stromal cell progesterone receptor (PGR), which is essential for decidual transformation. ZMIZ1 and ERα were co-localized in nuclei of mouse uterine cells, and E2F, CCNA2 and FOXM1 signaling were all decreased when ZMIZ1 was targeted, which likely underlies reduced cell cycle progression. Transcriptomic analyses revealed that loss of ZMIZ1 alters the amplitude of estrogen regulated gene responses, indicating ZMIZ1 fine-tunes endometrial cell signals needed for optimal functioning. Our findings demonstrate the importance of ZMIZ1 as an ERα co-regulator in uterine biology and pathology.
2025-09-22 | GSE288872 | GEO
Project description:The endometrial expression and activity of the transcriptional co-regulator, Zinc Finger MIZ-Type Containing 1 (Zmiz1), that is co-localized with a mouse uterine estrogen receptor α (ERα)-binding super-enhancer, has not yet been evaluated. In human endometrial biopsy samples ZMIZ1 transcript and protein is dynamically expressed during the menstrual cycle. ZMIZ1 mutations are associated with some uterine tumors and ZMIZ1 RNA levels are increased in endometrium from individuals with endometriosis. Disrupting ZMIZ1 in cultured human endometrial stromal cells or in mouse uterus prevented hormone-dependent proliferation of epithelial and stromal cells as well as decidual differentiation of stroma cells, triggering sterility. Additionally, aging-dependent fibrosis was accelerated in Zmiz1-targeted mouse uterus. Notably, ZMIZ1 deletion impacted expression of stromal cell progesterone receptor (PGR), which is essential for decidual transformation. ZMIZ1 and ERα were co-localized in nuclei of mouse uterine cells, and E2F, CCNA2 and FOXM1 signaling were all decreased when ZMIZ1 was targeted, which likely underlies reduced cell cycle progression. Transcriptomic analyses revealed that loss of ZMIZ1 alters the amplitude of estrogen regulated gene responses, indicating ZMIZ1 fine-tunes endometrial cell signals needed for optimal functioning. Our findings demonstrate the importance of ZMIZ1 as an ERα co-regulator in uterine biology and pathology.
2025-09-22 | GSE288879 | GEO
Project description:Transgenic mice expressing a truncated form of Zmiz1 in the skin develop spontaneous keratoacanthomas. In this experiment, a Cre-inducible transgene expressing a truncated form of Zmiz1 was introduced into mice. Activation of the transgene in these mice was achieved by breeding to K14-Cre transgenic animals. Double transgenic mice formed spontaenous keratoacanthomas with short latency. In this experiment, we generated gene expression profiles for five Zmiz1-induced keratoacanthomas and six normal skin samples.
2012-10-01 | E-GEOD-39360 | biostudies-arrayexpress
Project description:Polycomb repressive complex PRC1 is essential for gene regulation in numerous cell fate decisions. We show that RING1B (RING2, RNF2) and canonical PRC1 (cPRC1) genes are amplified and overexpressed in breast cancer (BC). Moreover, cPRC1 complexes functionally associate with genes regulated by cell type specific key transcription factors such as estrogen receptor (ER) in ER+ tumor cells and BRD4 in triple negative BC cells. cPRC1 is recruited to active enhancers in a manner independent of PRC2 and RING1B enzymatic activity. RING1B regulates enhancer activity and gene transcription not only by promoting the expression of BC oncogenes but also by regulating chromatin accessibility for oncogenic transcription factors. RING1B recruitment, and thus PRC1 association, to active enhancers occurs in multiple cancers.
2018-10-19 | PXD009570 | Pride
Project description:Human telomeres were one of the first discovered and characterized sequences forming quadruplex structures. Association of these structures with oncogenic and tumor suppressor proteins suggests their important role in cancer development and therapy efficacy. Since cationic porphyrin TMPyP4 is known as G-quadruplex stabilizer and telomerase inhibitor, the aim of the study was to analyze the anticancer properties of this compound in two different human breast-cancer MCF7 and MDA-MB-231 cell lines. The cytotoxicity of TMPyP4 alone or in combination with doxorubicin was measured by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromid) and clonogenic assays, and the cell-cycle alterations were analyzed by flow cytometry. Telomerase expression and activity were evaluated using qPCR and telomeric repeat amplification protocol (TRAP) assays, respectively. The contribution of G-quadruplex inhibitor to protein pathways engaged in cell survival, DNA repair, adhesion, and migration was performed using immunodetection. Scratch assay and functional assessment of migration and cell adhesion were also performed. Consequently, it was revealed that in the short term, TMPyP4 neither revealed cytotoxic effect nor sensitized MCF7 and MDA-MB-231 to doxorubicin, but altered breast-cancer cell adhesion and migration. It suggests that TMPyP4 might substantially contribute to a significant decrease in cancer cell dissemination and, consequently, cancer cell survival reduction. Importantly, this effect might not be associated with telomeres or telomerase.
| S-EPMC6600420 | biostudies-literature