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Targeted ErbB3 loss in mammary organoids harvested from ErbB3 DOX-KO mice +/- DOX treatment

ABSTRACT: Mammary organoids harvested from ErbB3 DOX-KO mice, which utilize MMTV-Cre transgene expression in the LE to cause genomic recombination at floxed ErbB3 alleles in ErbB3FL/FL were cultured in the presence or absence of doxycycline to induce ErbB3 loss. The gene expression shift following DOX-induced ErbB3 loss in the 3D organoids was examined by microarray. Gene expression patterns were interrogated in mammary organoids from ErbB3 inducible-knockout mice cultured in the presence of absence of doxycycline. Three biological replicates of the experiment were performed, resulting in a total of 6 samples (3 treatment, 3 control).

ORGANISM(S): Mus musculus

SUBMITTER: Justin Balko

PROVIDER: E-GEOD-32129 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The receptor tyrosine kinase ErbB3 maintains the balance between luminal and basal breast epithelium.

Balko Justin M JM Miller Todd W TW Morrison Meghan M MM Hutchinson Katherine K Young Christian C Rinehart Cammie C Sánchez Violeta V Jee David D Polyak Kornelia K Prat Aleix A Perou Charles M CM Arteaga Carlos L CL Cook Rebecca S RS

Proceedings of the National Academy of Sciences of the United States of America 20111216 1

ErbB3 harbors weak kinase activity, but strongly activates downstream phosphatidylinositol 3-kinase/Akt signaling through heterodimerization with and activation by other ErbB receptor tyrosine kinases. We report here that ErbB3 loss in the luminal mammary epithelium of mice impaired Akt and MAPK signaling and reduced luminal cell proliferation and survival. ERBB3 mRNA expression levels were highest in luminal mammary populations and lowest in basal cell/stem cell populations. ErbB3 loss in mamma ...[more]

PMID: 22178756

Similar Datasets

Targeted ErbB3 loss in mammary organoids harvested from ErbB3 DOX-KO mice +/- DOX treatment

Project description:Mammary organoids harvested from ErbB3 DOX-KO mice, which utilize MMTV-Cre transgene expression in the LE to cause genomic recombination at floxed ErbB3 alleles in ErbB3FL/FL were cultured in the presence or absence of doxycycline to induce ErbB3 loss. The gene expression shift following DOX-induced ErbB3 loss in the 3D organoids was examined by microarray.

2012-01-04 | GSE32129 | GEO

Analysis of Liver Progenitor Cells Generated from Yap Expression [Set 1]

Project description:Hippo signaling is highly associated with activity in the stem cell compartment of many epithelial tissues. In this study, we examined if Hippo signaling inhibition (by inducing Yap expression) could convert differentiated cells into a progenitor like phenotype. Organoid cells derived from mouse livers under various conditions, wild-type, Yap ON (Plus Dox), and Yap ON then OFF (Minus Dox) was examined. Comparison between freshly isolated hepatocytes; Uninduced_YPF-#.cel against Organoids grown in wild-type conditions (WT), Yap On (in vivo) off (in vitro) - YapOrganoidDoxMinus , and Yap On continuously - YapOrganoidDoxPlus. Organoids grown in culture or YFP+ sorted liver cells after the indicated time of Yap expression were collected. These were amplified using Nugene technology and hybridized to Affymetrix MoGene1.0 st arrays.

2014-06-06 | E-GEOD-55558 | biostudies-arrayexpress

Mus musculus

Project description:Targeted ErbB3 loss in mammary organoids harvested from ErbB3 DOX-KO mice +/- DOX treatment

| PRJNA147437 | ENA

Transcription profiling of transgenic mice (tTA/IkappaBalpha-AA) treated with doxycycline (DOX), which represses expression of the transgenic IkappaBalpha

Project description:double transgenic mice (tTA/IkappaBalpha-AA) were treated with doxycycline (DOX), which represses expression of the transgenic IkappaBalpha. Double transgenic mice without Dox-treatment overexpress the transdominant IkappaBalpha, which represses NFkappaB activation.

2006-05-10 | E-MEXP-358 | biostudies-arrayexpress

RNA-seq analysis of doxycycline-regulated gene expression in Aspergillus fumigatus cells containing a dox off-ffmA fusion gene.

Project description:To determine the genes responsive to FfmA in A. fumigatus, a doxycycline-repressible (dox off) gene fusion to the ffmA coding sequence was constructed. This strain was designated SPF182. These cells were grown for 16 hours in the absence of doxycycline and then shifted into medium containing doxycycline (+dox) or untreated (-dox). After 8 additional hours, the cells were harvested and total RNA prepared. Wild-type cells were grown in parallel as a control in -dox medium.

2023-07-26 | GSE229912 | GEO

EWS-FLI1-induced osteosarcoma model unveiled a crucial role of impaired osteogenic differentiation on osteosarcoma development [gene expression]

Project description:EWS-FLI1, a multi-functional fusion oncogene, is exclusively detectable in Ewing sarcomas. However, previous studies reported that a subset of osteosarcomas also harbor EWS-ETS family fusion, suggesting that the fusion gene may be involved in the development of a particular type of osteosarcomas. Here using the doxycycline inducible EWS-FLI1 system, we established an EWS-FLI1-dependent osteosarcoma model from murine bone marrow stromal cells. We revealed that the withdrawal of EWS-FLI1 expression enhances the osteogenic differentiation of sarcoma cells, leading to mature bone formation. Taking advantage of induced pluripotent stem cell (iPSC) technology, we also showed that the sarcoma-derived iPSCs with cancer-related genetic abnormalities exhibited the impaired differentiation program of osteogenic lineage irrespective of the EWS-FLI1 expression. Finally, we demonstrated that EWS-FLI1 contributed to in vitro sarcoma development from the sarcoma-iPSCs after osteogenic differentiation. These findings demonstrated that modulating cellular differentiation is fundamental principle of the EWS-FLI1-induced osteosarcoma development. Furthermore, the in vitro cancer model using sarcoma-iPSCs should provide a novel platform for dissecting relationship between cancer genome and cellular differentiation. Microarray in mouse EWS-FLI1-induced osteosarcoma cell lines(SCOS#2 and SCOS#12) and sarcoma(SCOS#2)-derived iPSCs. Total 6 samples were analyzed. We can induce EWS-FLI1 expression by Doxycycline-inducible expression system in SCOS#2 and #12. We investigaed EWS-FLI1 activated genes (Dox ON-High) and EWS-FLI1 repressed genes (Dox OFF-High) in SCOS#2 and #12 sarcoma cell lines. Also, we investigated global gene expression pattern of sarcoma-derived iPSCs (iPSC#2-A1 and #2-B5). A link to this sample file can be found below.

2016-03-01 | E-GEOD-72704 | biostudies-arrayexpress

Quantitative proteomics to systematically assess protein changes after HUWE1 knockout, in RAW264.7-Dox-Cas9.

Project description:Quantitative proteomics to systematically assess protein changes after HUWE1 knockout, in RAW264.7-Dox-Cas9.

2023-03-22 | PXD036715 | Pride

murine MYC-dependent lymphoma cells: Dox vs. NoDox treatment

Project description:miRNA expression profiling of murine MYC-dependent lymphoma cell lines harboring the MYC-transgene in a Tet-off system comparing control untreated lymphoma cells (high MYC expression state) with 18hours Dox treated lymphoma cells (low MYC expression state). Keywords: inducible expression system Two-condition experiment, Dox vs. NoDox treatment. Biological replicates: 26 distinct cell lines, 1 technical replicate. Four replicates per array.

2010-05-25 | E-GEOD-12394 | biostudies-arrayexpress

Retinoic acid and Azakenpoullone treatment in SH-SY5Y/6TR(EU)/pTrex-Dest-30/MYCN cell line in high and low MYCN levels

Project description:The effect of the GSK3 inhibitor Azakenpaullone (Azak) and the differentiation agent retinoic acid (RA) was studied in low and high MYCN levels in the MYCN inducible neuroblastoma cell line SH-SY5Y/6TR(EU)/pTrex-Dest-30/MYCN (SY5Y-MYCN). Azak was dissolved in DMSO in order to apply it to the cells. Therefore a vehicle control consisting of SY5Y-MYCN cells treated with 24h 1 ul/ml DMSO only was used in duplicates. Doxycycline (Sigma) dissolved in water was used at a final concentration of 1ug/ml to induce MYCN expression in SY5Y-MYCN. A co-treatment study with Dox and Azak was conducted. SY5Y-MYCN cells were treated with 24h Azak, 24h Azak & 48h Dox and 48h Dox, with biological duplicates. 1 uM RA (dissolved in DMSO) and 1 ug/mL Doxycycline were given individually and in combination. SY5Y-MYCN cells were treated with 24h RA, 24h RA & 48h Dox, and 48h Dox and RNA was extracted in biological duplicates. For the 24h RA & 48h Dox co-treatment cells were treated with Dox for 24h and then with RA and fresh Dox for a further 24h.

2015-06-30 | E-MTAB-2689 | biostudies-arrayexpress

NRG1/ERBB3 signaling in melanocyte Melan-Ink4a cells

Project description:Neuregulin (NRG) signaling through the receptor tyrosine kinase, ERBB3, is required for embryonic development, and dysregulated signaling has been associated with cancer progression. Here, we show that NRG1/ERBB3 signaling inhibits melanocyte (MC) maturation and promotes undifferentiated, migratory and proliferative cellular characteristics. Embryonic analyses demonstrated that initial MC specification and distribution were not dependent on ERBB3 signaling. However NRG1/ERBB3 signaling was both necessary and sufficient to inhibit differentiation of later stages of MC development in culture. Analysis of tissue arrays of human melanoma samples suggests that ERBB3 signaling may also contribute to metastatic progression of melanoma as ERBB3 was phosphorylated in primary tumors compared with nevi or metastatic lesions. Neuregulin 1-treated MCs demonstrated increased proliferation and invasion and altered morphology concomitant with decreased levels of differentiation genes, increased levels of proliferation genes and altered levels of melanoma progression and metastases genes. ERBB3 activation in primary melanomas suggests that NRG1/ERBB3 signaling may contribute to the progression of melanoma from benign nevi to malignancies. We propose that targeting ERBB3 activation and downstream genes identified in this study may provide novel therapeutic interventions for malignant melanoma.

2010-04-26 | GSE21463 | GEO

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