High Dose Tamoxifen in the Mouse Gastric Epithelium
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE71580 | GEO | 2015/07/31
SECONDARY ACCESSION(S): PRJNA291541
REPOSITORIES: GEO
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Project description:Tamoxifen, a selective estrogen receptor modulator, is widely used in research and clinically in patients. Tamoxifen injection (3 consecutive days, intraperitoneal, 5mg/20g mouse body weight) causes dramatic rearrangement of the gastric mucosa with loss of > 90% of PCs, a 6-fold increase in proliferation in stem/progenitor cells, and morphological changes in the ZCs in the bases of gastric-units. Time course of injection of high-dose tamoxifen. 3 mice were pooled for each condition.
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Project description:We are investigating the mRNA expression profiles of gastric tissue within H. pylori-infected mice treated with estradiol, tamoxifen, or placebo We used microarrays to compare the global mRNA expression profiles in H. pylori infected mice in response to estradiol and tamoxifen Male mice were infected with H. pylori. After 16 weeks of H.pylori infection, mice were treated with 17beta-estradiol, Tamoxifen or placebo pellets implated subcutaneously for 12 weeks. At that point, longitudinal strips of gastric tissue were snap-frozen. Tissue was later weighed and RNA extracted using Trizol and purified with RNeasy kit including DNase treatment. 9 samples with 3 groups (n= 3 per group, except Tamoxifen (n=2)). Placebo samples are controls and were compared to estradiol or Tamoxifen treated samples.
2011-06-30 | E-GEOD-29715 | biostudies-arrayexpress
Project description:We are investigating the mRNA expression profiles of gastric tissue within H. pylori-infected mice treated with estradiol, tamoxifen, or placebo We used microarrays to compare the global mRNA expression profiles in H. pylori infected mice in response to estradiol and tamoxifen
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Project description:Tmem100 was identified as a downstream gene of BMP9-ALK1 signaling. The signaling has been implicated in hereditary hemorrhagic telangiectasia. This study was designed to identify affected genes in TMEM100-deficiect mice. Tmem100 was inactivated in adult Tmem1002loxP/2loxP;ROSA26+/CreER mice by tamoxifen tereatment. Microarray data was obtained from the lungs isolated from tamoxifen treated control and mutant mice. Three control mice (Tmem1002loxP/2loxP) and three mutant mice (Tmem1002loxP/2loxP;ROSA26+/CreER) were treated with tamoxifen (two consecutive intraperitoneal injections, 0.1 mg/g of body weight) to activate CreER recombinase. Total RNAs were isolated from lungs 7 days after tamoxifen injection.
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Project description:Our microbiota affects numerous processes involved in development, health, and the response to chemotherapeutic drugs. Tamoxifen is a selective estrogen receptor (ER) modulator that is used to treat ER positive breast cancer, but that at high doses kills both ER positive and ER-negative breast cancer cells. We recapitulate this off-target effect in Caenorhabditis elegans, which does not have an ER ortholog. We find that different bacteria dramatically modulate tamoxifen toxicity in C. elegans, with a three-order of magnitude difference between animals fed Escherichia coli, Comamonas aquatica, and Bacillus subtilis. Remarkably, host fatty acid (FA) biosynthesis mitigates tamoxifen toxicity, and different bacteria provide the animal with different FAs, resulting in distinct FA profiles. Surprisingly these bacteria modulate tamoxifen toxicity by different death mechanisms, some of which are modulated by FA supplementation and others by antioxidants. Together, this work reveals a complex interplay between bacteria, FA metabolism and tamoxifen toxicity that may provide a blueprint for similar studies in more complex mammals.
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Project description:To directly examine the role of Foxe1 in the adult thyroid we generated a model of tamoxifen-inducible Cre mediated Foxe1 deletion in mice of C57BL/6J background (Foxe1flox/flox/Cre). Tamoxifen (0.05g/kg) was administered intraperitoneally to Foxe1flox/flox/Cre mice or Cre control mice aged 6-8 weeks, once daily for five consecutive days. Thyroids were harvested two weeks post-treatment, total RNA extracted and transcriptomic analysis performed using Clariom S Mouse arrays.
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Project description:Tamoxifen, a selective estrogen receptor modulator (SERM), is commonly used in the treatment of hormone-responsive cancers. The effects of tamoxifen in anabolic tissues harboring estrogen-receptors, such as skeletal muscle, are poorly understood. As estrogen and estrogen receptors play an important role in skeletal muscle development and repair, we hypothesize that tamoxifen may have specific effects on myogenesis, the developmental process underlying muscle cells differentiation and repair. Myogenesis is characterized by fine-tuned changes in protein expression as embryonic myoblasts and adult satellite cells transition from pluripotent stem cells to multinucleated, contractile muscle fibers: we undertake a quantitative proteomic analysis of tamoxifen-induced changes in developing skeletal muscle cells which we expect may also shed light on the effect of tamoxifen on muscle repair.
We report a tandem mass-tag (TMT) approach to tamoxifen-treated myogenesis in C2C12 cells, a well-characterized model of in vitro murine skeletal muscle differentiation. A longitudinal analysis of >10,000 proteins identified in C2C12 myogenesis revealed a novel subset of 1,239 myogenically-regulated proteins. This set of regulatory proteins clustered into five distinct longitudinal expression trends which significantly overlap those obtained in similar analyses performed in human myocytes. A longitudinal analysis of myogenesis in the presence of tamoxifen, when contrasted with a similar analysis in untreated myogenesis finds that while the vast majority of myogenically-regulated proteins were unaffected by tamoxifen treatment, specific pathways and networks are affected. We document a specific functional enrichment for adiponectin-signaling, whereby a set of 198 proteins were differentially expressed relative to controls at one or more stages of myogenesis, the majority of which were involved in steroid biosynthesis, lipid storage and/or metal ion homeostasis. Interestingly, the only protein that was differentially expressed in the tamoxifen-treated cells at every stage of myogenesis was metallothionein-1 (MT1). Elevated levels of MT1 have been correlated with tamoxifen resistance and increased patient mortality and relapse in breast cancer, as well as with cachexia and muscle atrophy in rodent models. Increased MT1 expression levels may contribute to the musculoskeletal effects reported by patients undergoing tamoxifen treatment. Finally, we present a powerful, self-validating pipeline for analyzing the total proteomic response to in vitro treatment across every stage of muscle cells development which can be easily adapted to study the effects of other drugs on myogenesis.
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Project description:The beneficial effect of the selective estrogen receptor modulator (SERM) tamoxifen in the treatment and prevention of breast cancer is assumed to be through its ability to antagonize the stimulatory actions of estrogen, although tamoxifen can also have some estrogen-like agonist effects. Here we report that in addition to these mixed agonist/antagonist actions, tamoxifen can also selectively regulate a unique set of more than 60 genes in estrogen receptor alpha (ERa)-positive MCF-7 human breast cancer cells which are minimally regulated by estradiol or raloxifene. This gene regulation by tamoxifen is mediated by ERa and is reversed by estradiol or ICI 182,780. We find that the introduction of ERbeta into MCF-7 cells reverses tamoxifen action on approximately 75% of these genes, suggesting that ERbeta is capable of repressing certain actions of tamoxifen. To examine whether these genes might serve as markers of tamoxifen sensitivity and/or the development of resistance, the expression level of these genes was examined in breast tumors of women who had received treatment with tamoxifen. High expression of two of the tamoxifen stimulated genes, YWHAZ/14-3-3z and LOC441453, was found to correlate significantly with disease recurrence following tamoxifen treatment in women with ER-positive tumors, and hence appear to be markers of a poor prognosis. Our data indicate a new dimension in tamoxifen action, involving gene expression regulation that is tamoxifen-preferential, and identify genes that might serve as markers of tumor responsiveness or resistance to tamoxifen therapy. Keywords: ligand response in two ER backgrounds
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