Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384522 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This experiment is performed to reveal the novel binding sites of ZEB1 transcription factor globally in triple negative breast cancer cell line Hs578T. We also reveal the effect of TGF cytokine on the binding sites of ZEB1.
2018-04-25 | E-MTAB-5241 | biostudies-arrayexpress
Project description:ZEB1 binding sites in TGF-beta-stimulated MDA-231-D and Hs578T basal type breast cancer cell lines [ChIP-seq]
| PRJNA350681 | ENA
Project description:Grainyhead genes are involved in wound healing and developmental neural tube closure. In light of the high degree of similarity between the epithelial-mesenchymal transitions (EMTs) occurring in wound healing processes and the cancer stem cell-like compartment of tumors, including TGF-β-dependence, we investigated the role of a Grainyhead gene (GRHL2) in oncogenic EMT. Grainyhead was specifically down-regulated in the claudin-low subclass of mammary tumors and in the basal-B subclass of breast cancer cell lines. Functionally, GRHL2 suppressed TGF-β-induced, Twist-induced or spontaneous EMT, enhanced anoikis-sensitivity, and suppressed mammosphere generation in mammary epithelial cells. These effects were mediated, in part, by its suppression of ZEB1 expression, through direct repression of the ZEB1 promoter. GRHL2 also inhibited Smad-mediated transcription, and up-regulated mir200b/c as well as the TGF-β receptor antagonist, BMP2. The expression of GRHL2 in the breast cancer cell line MDA-MB-231 triggered a mesenchymal-to-epithelial transition and sensitized the cells to anoikis. These results indicate that GRHL2 is a suppressor of the oncogenic EMT. 3 biologic replicates for each cell line. Comparison of HMLE+Twist-ER cells expressing GRHL2/pMIG vs. HMLE+Twist-ER cells expressing empty pMIG.
2012-02-25 | E-GEOD-36081 | biostudies-arrayexpress
Project description:Identification of DNA binding sites of the transcription factor ZEB1 in the human breast cancer cell line MDA-MB-231 by chromatin-immunoprecipitation followed by sequencing (ChIP-seq).
2020-07-22 | E-MTAB-8258 | biostudies-arrayexpress
Project description:Long non-coding RNAs (lncRNAs) are critical regulators in cancer. However, the involvement of lncRNAs in TGF-beta-regulated tumorigenicity is still unclear. Here we identify TGF-beta-activated lncRNA LINC00115 as a critical regulator in glioma stem-like cell (GSC) self-renewal and tumorigenicity. LINC00115 is upregulated by TGF-beta, acts as a miRNA sponge and upregulates ZEB1 by competitively binding miR-200s, thereby enhancing ZEB1 signaling and GSC self-renewal.
2019-09-08 | GSE134595 | GEO
Project description:The epithelial to mesenchymal transition (EMT) is implicated in the metastatic spread of breast cancer cells. EMT transcription factors (TF) regulate different stages of EMT states. In breast cancers, estrogen receptor α (ERα) maintains the epithelial characteristics of breast tumors and is indispensable for efficient endocrine therapy. In this study we investigate whether and how ZEB1, an EMT-TF affects ERα signaling at early stages of EMT and metastasis. We did ERα ChIP-seq in wild type MCF7-V cells for comparative studies. We also did ERα ChIP-seq in cells stably expressing a doxycycline-inducible construct to express ZEB1. This was to determine the impact of ZEB1 on the ERα cistrome in MCF7-V breast cancer cells induced with DMSO, 17-beta estradiol (E2), and forskolin + 3-isobutyl-1-methylxanthine (IBMX) (FI).
2022-03-14 | GSE173479 | GEO
Project description:Grainyhead genes are involved in wound healing and developmental neural tube closure. In light of the high degree of similarity between the epithelial-mesenchymal transitions (EMTs) occurring in wound healing processes and the cancer stem cell-like compartment of tumors, including TGF-β-dependence, we investigated the role of a Grainyhead gene (GRHL2) in oncogenic EMT. Grainyhead was specifically down-regulated in the claudin-low subclass of mammary tumors and in the basal-B subclass of breast cancer cell lines. Functionally, GRHL2 suppressed TGF-β-induced, Twist-induced or spontaneous EMT, enhanced anoikis-sensitivity, and suppressed mammosphere generation in mammary epithelial cells. These effects were mediated, in part, by its suppression of ZEB1 expression, through direct repression of the ZEB1 promoter. GRHL2 also inhibited Smad-mediated transcription, and up-regulated mir200b/c as well as the TGF-β receptor antagonist, BMP2. The expression of GRHL2 in the breast cancer cell line MDA-MB-231 triggered a mesenchymal-to-epithelial transition and sensitized the cells to anoikis. These results indicate that GRHL2 is a suppressor of the oncogenic EMT.
2012-02-25 | GSE36081 | GEO
Project description:Transforming growth factor-β (TGF-β) comprises a key component in the tumor microenvironment. It is reported that TGF-β can be pro-tumorigenic or anti-tumorigenic depending on various contexts. Some of the triple negative breast cancers highly express TGF-β, but pro-tumorigenic function of TGF-β in triple negative breast cancer cells is not fully known. Therefore, we analyzed genome-wide gene expression changes after stimulation with TGF-β in a triple negative breast cancer cell line, Hs578T cells.
2020-12-24 | GSE152414 | GEO
Project description:The epithelial to mesenchymal transition (EMT) is implicated in the metastatic spread of breast cancer cells. EMT transcription factors (TF) regulate different stages of EMT states. In breast cancers, estrogen receptor α (ERα) maintains the epithelial characteristics of breast tumors and is indispensable for efficient endocrine therapy. In this study we investigate whether and how ZEB1, an EMT-TF affects ERα signaling at early stages of EMT and metastasis. In MCF7-V cells, we used RNA-seq to study the impact of ZEB1 on the ERα transcriptome in breast cancer cells induced with DMSO, 17-beta estradiol (E2), and forskolin + 3-isobutyl-1-methylxanthine (IBMX) (FI).
2022-03-14 | GSE173484 | GEO
Project description:Transforming growth factor (TGF)-beta induces apoptosis of many types of cancer cells and acts as a tumor suppressor. We found lower expression of TGF-beta type II receptor (TbRII) in most of SCLC cells and tissues than in normal lung epithelial cells and normal lung tissues, respectively. In vitro cell growth and in vivo tumor formation were suppressed by TGF-beta-mediated apoptosis when the wild-type TbRII was overexpressed in SCLC cells. We therefore determined Smad2 and Smad3 (Smad2/3) binding sites in a SCLC cell line H345 stably expressing exogenous TbRII (H345-TbRII) to identify target genes of TGF-beta. Smad2 and Smad3 binding sites in H345-TbRII cells were determined by ChIP-seq (one sample analysis, without replicates).
2015-09-15 | E-GEOD-63871 | biostudies-arrayexpress