Gene expression profiling: cell cycle deregulation and aneuploidy do not cause breast cancer formation in WAP-SVT/t transgenic animals

Klein, Andreas; Guhl, Eva; Zollinger, Raphaël; Tzeng, Yin-Jeh; Wessel, Ralf; Hummel, Michael; Graessmann, M.; Graessmann, A.

doi:10.1007/s00109-004-0625-1

Cited by 24 publications

(31 citation statements)

References 28 publications

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“…“Rapid Increase” genes (A): Growth arrest-specific 6 (Gas6) is mitogenic in a mammary cell line (Goruppi et al 2001; Varnum et al 1995) and its expression is regulated by estradiol in mouse mammary epithelial cells (Mo et al 2007). The expression of procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (Plod2) , which catalyzes the hydroxylation of lysyl residues in collagen-like peptides, increases during pubertal mammary development (McBryan et al 2007) and is elevated in mammary tumors in WAP-SVT/t transgenic mice (Klein et al 2005). The extracellular matrix protein, cartilage intermediate layer protein (Cilp) is upregulated by estradiol in ERα-expressing osteosarcoma cells (Klein et al 2005).…”

Section: Resultsmentioning

confidence: 99%

Profile of estrogen‐responsive genes in an estrogen‐specific mammary gland outgrowth model

Deroo

Hewitt

Collins

et al. 2009

Molecular Reproduction Devel

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Both ovarian and pituitary hormones are required for the pubertal development of the mouse mammary gland. Estradiol directs ductal elongation and branching, while progesterone leads to tertiary branching and alveolar development. The purpose of this investigation was to identify estrogen-responsive genes associated with pubertal ductal growth in the mouse mammary gland in the absence of other ovarian hormones and at different stages of development. We hypothesized that the estrogen-induced genes and their associated functions at early stages of ductal elongation would be distinct from those induced after significant ductal elongation had occurred. Therefore, ovariectomized prepubertal mice were exposed to 17β-estradiol from two to twenty-eight days, and mammary gland global gene expression analyzed by microarray analysis at various times during this period. We found that: a) gene expression changes in our estrogen-only model mimic those changes that occur in normal pubertal development in intact mice, and b) both distinct and overlapping gene profiles were observed at varying extents of ductal elongation, and c) cell proliferation, the immune response, and metabolism/catabolism were the most common functional categories associated with mammary ductal growth. Particularly striking was the novel observation that genes active during carbohydrate metabolism were rapidly and robustly decreased in response to estradiol. Lastly, we identified mammary estradiol-responsive genes that are also co-expressed with Estrogen Receptor α in human breast cancer. In conclusion, our genomic data support the physiological observation that estradiol is one of the primary hormonal signals driving ductal elongation during pubertal mammary development.

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Section: Resultsmentioning

confidence: 99%

Profile of estrogen‐responsive genes in an estrogen‐specific mammary gland outgrowth model

Deroo

Hewitt

Collins

et al. 2009

Molecular Reproduction Devel

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“…For antibodies, see Supplementary Methods. Specificity of the STEAP1 antibody was assessed previously (21,22).…”

Section: Western Blottingmentioning

confidence: 99%

STEAP1 Is Associated with the Invasive and Oxidative Stress Phenotype of Ewing Tumors

Grünewald

Diebold

Espósito

et al. 2012

Molecular Cancer Research

114

132

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Ewing tumors comprise the second most common type of bone-associated cancer in children and are characterized by oncogenic EWS/FLI1 fusion proteins and early metastasis. Compelling evidence suggests that elevated levels of intracellular oxidative stress contribute to enhanced aggressiveness of numerous cancers, possibly including Ewing tumors. Using comprehensive microarray analyses and RNA interference, we identified the six-transmembrane epithelial antigen of the prostate 1 (STEAP1)-a membrane-bound mesenchymal stem cell marker of unknown function-as a highly expressed protein in Ewing tumors compared with benign tissues and show its regulation by EWS/FLI1. In addition, we show that STEAP1 knockdown reduces Ewing tumor proliferation, anchorage-independent colony formation as well as invasion in vitro and decreases growth and metastasis of Ewing tumor xenografts in vivo. Moreover, transcriptome and proteome analyses as well as functional studies revealed that STEAP1 expression correlates with oxidative stress responses and elevated levels of reactive oxygen species that in turn are able to regulate redox-sensitive and proinvasive genes. In synopsis, our data suggest that STEAP1 is associated with the invasive behavior and oxidative stress phenotype of Ewing tumors and point to a hitherto unanticipated oncogenic function of STEAP1. Mol Cancer Res; 10(1); 52-65. Ó2011 AACR.

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“…Expression values obtained were adjusted to the intensity of the corresponding expression value of 100 housekeeping genes. Transcripts with average signal values lower than the minimum threshold of 50 arbitrary units were excluded (Klein et al, 2005).…”

Section: Cell Culturementioning

confidence: 99%

Chemotherapy resistance of mouse WAP-SVT/t breast cancer cells is mediated by osteopontin, inhibiting apoptosis downstream of caspase-3

et al. 2006

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Gene expression profiling: cell cycle deregulation and aneuploidy do not cause breast cancer formation in WAP-SVT/t transgenic animals

Cited by 24 publications

References 28 publications

Profile of estrogen‐responsive genes in an estrogen‐specific mammary gland outgrowth model

Profile of estrogen‐responsive genes in an estrogen‐specific mammary gland outgrowth model

STEAP1 Is Associated with the Invasive and Oxidative Stress Phenotype of Ewing Tumors

Chemotherapy resistance of mouse WAP-SVT/t breast cancer cells is mediated by osteopontin, inhibiting apoptosis downstream of caspase-3

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