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Changes in gene expression during acinar morphogenesis of normal-like human mammary epithelial cells in a 3D basement membrane cultures

ABSTRACT: In this study, we examined temporal changes in gene expression during acinar morphogenesis of normal-like human mammary epithelial cells (MCF-10A) in a three-dimensional (3D) basement membrane cultures.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33354 | GEO | 2013/12/01

SECONDARY ACCESSION(S): PRJNA149031

REPOSITORIES: GEO

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Changes in gene expression during acinar morphogenesis of normal-like human mammary epithelial cells in a 3D basement membrane cultures

Project description:In this study, we examined temporal changes in gene expression during acinar morphogenesis of normal-like human mammary epithelial cells (MCF-10A) in a three-dimensional (3D) basement membrane cultures. Changes in gene expression in 3D culture of MCF-10A cells were measured at 4, 8, and 12 days.

2013-12-01 | E-GEOD-33354 | biostudies-arrayexpress

Nanolipoprotein mediated Her2 protein transfection induces malignant transformation in human breast acinar cultures

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Specific 3-O-sulfated heparan sulfate domains regulate salivary gland basement membrane metabolism and epithelial differentiation [female]

Project description:FGF signaling is essential for salivary gland (SG) development and heparan sulfate (HS) regulation of FGFR function is determined by immense structural diversity of sulfated HS domains. The basement membrane (BM), containing HS proteoglycans, collagens and laminins, separates epithelia from stroma and controls growth factor-matrix cross-talk. 3-O-sulfotransferases generate highly 3-O-sulfated HS domains (3-O-HS) and Hs3st3a1 and Hs3st3b1 are enriched in myoepithelial cells (MECs), which produce BM and are a growth factor signaling hub. To investigate 3-O-HS regulation of MEC function and growth factor signaling, we generated Hs3st3a1;Hs3st3b1 double knockout (DKO) mice. The DKO HS loses specific highly 3-O-sulfated tetrasaccharides, which increases FGF/FGFR-complex binding to HS. During development this leads to increased FGFR-, BM- and MEC-related gene expression. However, in adult DKO SGs the secretory units containing acinar and MECs, have reduced MECs, increased BM and disrupted acinar polarity, resulting in salivary hypofunction. We used defined 3-O-sulfated-HS in FGFR pulldown assays and primary organ cultures to investigate 3-O-HS-dependent mechanisms regulating MEC development. We find that 3-O-HS modulates FGFR signaling to regulate MEC BM synthesis which is critical for secretory unit homeostasis and acinar function. Understanding how sulfated HS regulates development will inform the use of HS mimetics in organ regeneration.

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Specific 3-O-sulfated heparan sulfate domains regulate salivary gland basement membrane metabolism and epithelial differentiation [male]

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Gene expression profile of a C. elegans Anchor cell invading through Basement Membrane

Project description:Cell invasion through basement membrane is crucial for development and immune cell trafficking, and is misregulated in many human diseases, such as cancer. Understanding the gene expression profile of invading cells is challening, because cell invasion events are often stochastic and rare. Thus, it has been difficult to isolate cells during the act of basement membrane invasion. Here, we have taken advantage of the stereotyped timing of anchor cell invasion in C. elegans, along with synchronized animal culturing, Fluorescence activated cell sorting (FACS), and RNA-Seq and identified the gene expression profile of an invasive cell at the time of basement membrane breaching.

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Effects of a Tricaprylin Emulsion on Anti-glomerular Basement Membrane Glomerulonephritis in Rats

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Effects of a Tricaprylin Emulsion on Anti-glomerular Basement Membrane Glomerulonephritis in Rats

Project description:Expression data from rat with anti-glomerular basement membrane nephritis (anti-GBM). We used microarrays to analyze the transcriptome of kidney from anti-GBM model rat with or without drug treatment RNA from whole kidneys was extracted and processed for hybridization on Affymetrix microarrays.

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Mutant p53 Disrupts Mammary Acinar Morphogenesis via the Mevalonate Pathway

Project description:p53 is a frequent target for mutation in human tumors and previous studies have revealed that these missense mutant proteins can actively contribute to tumorigenesis. To elucidate how mutant p53 might contribute to mammary carcinogenesis we employed a three-dimensional (3D) culture model. In 3D culture non-malignant breast epithelial cells form structures reminiscent of acinar structures found in vivo, whereas breast cancer cells form highly disorganized and in some cases invasive structures. We found that mutant p53 depletion is sufficient to phenotypically revert breast cancer cells to a more acinar-like morphology. Genome-wide expression analysis identified the sterol biosynthesis, or mevalonate, pathway as significantly upregulated by a tumor-derived mutant p53. Using statins and sterol biosynthesis intermediates, we demonstrate that this pathway is both necessary and sufficient for the phenotypic effects of mutant p53 on breast tissue architecture. Mutant p53 associates with the sterol gene promoters at least partly via the SREBP transcription factors. Finally, p53 mutation correlates with higher levels of sterol biosynthesis genes in human breast tumors. This activity of mutant p53 not only contributes insight into breast carcinogenesis, but also implicates the mevalonate pathway as a new therapeutic target for tumors bearing such mutations in p53. RNA was isolated from three independent experiments of MDA-468.shp53 cells cultured under 3D conditions for 8 days in the presence or absence of DOX, reversed transcribed and hybridized to an Affymetrix GeneChip expression array. Data was processed using the Robust Multichip Average (RMA) algorithm to give expression signals and paired t-test was applied for each probe. Probes with 1% significance were selected for Ingenuity Pathway Analysis.

2012-02-13 | E-GEOD-31812 | biostudies-arrayexpress

Optic cup morphogenesis requires neural crest-mediated basement membrane assembly.

Project description:Organogenesis requires precise interactions between a developing tissue and its environment. In vertebrates, the developing eye is surrounded by a complex extracellular matrix as well as multiple mesenchymal cell populations. Disruptions to either the matrix or periocular mesenchyme can cause defects in early eye development, yet in many cases the underlying mechanism is unknown. Here, using multidimensional imaging and computational analyses in zebrafish, we establish that cell movements in the developing optic cup require neural crest. Ultrastructural analysis reveals that basement membrane formation around the developing eye is also dependent on neural crest, but only specifically around the retinal pigment epithelium. Neural crest cells produce the extracellular matrix protein nidogen: impairing nidogen function disrupts eye development, and, strikingly, expression of nidogen in the absence of neural crest partially restores optic cup morphogenesis. These results demonstrate that eye formation is regulated in part by extrinsic control of extracellular matrix assembly.This article has an associated 'The people behind the papers' interview.

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Mutant p53 Disrupts Mammary Acinar Morphogenesis via the Mevalonate Pathway

2012-02-13 | GSE31812 | GEO