Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Bisphenol A Exposure and Multiple Sclerosis Risk

ABSTRACT: Bisphenol A Exposure and Multiple Sclerosis Risk Comparison of vehicle-treated vs. BPA-treated mouse testes tissue. Each comparison in technical and biological duplicate (Done twice: total 4 replicates)

ORGANISM(S): Mus musculus

SUBMITTER: Anne Katchy

PROVIDER: E-GEOD-45917 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Studies in experimental autoimmune encephalomyelitis do not support developmental bisphenol a exposure as an environmental factor in increasing multiple sclerosis risk.

Krementsov Dimitry N DN Katchy Anne A Case Laure K LK Carr Frances E FE Davis Barbara B Williams Cecilia C Teuscher Cory C

Toxicological sciences : an official journal of the Society of Toxicology 20130623 1

Multiple sclerosis (MS), a demyelinating immune-mediated central nervous system disease characterized by increasing female penetrance, is the leading cause of disability in young adults in the developed world. Epidemiological data strongly implicate an environmental factor, acting at the population level during gestation, in the increasing incidence of female MS observed over the last 50 years, yet the identity of this factor remains unknown. Gestational exposure to bisphenol A (BPA), an endocri ...[more]

PMID: 23798566

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Project description:The estrogen receptor (ER)M-NM-21 is successively lost during cancer progression, whereas its splice variant, ERM-NM-22, is expressed in advanced prostate cancer. The latter form of cancer often metastasizes to bone, and we wanted to investigate whether the loss of ERM-NM-21 and/or the expression of ERM-NM-22 affect such signaling pathways in prostate cancer. Using PC3 and 22Rv1 prostate cancer cell lines that stably express ERM-NM-21 or ERM-NM-22, we found that the ERM-NM-2 variants differentially regulate genes known to affect tumor behavior. We found that ERM-NM-21 repressed the expression of the bone metastasis regulator Runx2 in PC3 cells. By contrast, RUNX2 expression was up-regulated at the mRNA level by ERM-NM-22 in PC3 cells, whereas Slug was up-regulated by ERM-NM-22 in both PC3 and 22Rv1 cells. In addition, the expression of Twist1, a factor whose expression strongly correlates with high Gleason grade prostate carcinoma, was increased by ERM-NM-22. In agreement with the increased Twist1 expression, we found increased expression of Dickkopf homolog 1; Dickkopf homolog 1 is a factor that has been shown to increase the RANK ligand/osteoprotegerin ratio and enhance osteoclastogenesis, indicating that the expression of ERM-NM-22 can cause osteolytic cancer. Furthermore, we found that only ERM-NM-21 inhibited proliferation, whereas ERM-NM-22 increased proliferation. The expression of the proliferation markers Cyclin E, c-Myc, and p45(Skp2) was differentially affected by ERM-NM-21 and ERM-NM-22 expression. In addition, nuclear M-NM-2-catenin protein and its mRNA levels were reduced by ERM-NM-21 expression. In conclusion, we found that ERM-NM-21 inhibited proliferation and factors known to be involved in bone metastasis, whereas ERM-NM-22 increased proliferation and up-regulated factors involved in bone metastasis. Thus, in prostate cancer cells, ERM-NM-22 has oncogenic abilities that are in strong contrast to the tumor-suppressing effects of ERM-NM-21. The GFP vs. ERbeta1 comparison was carried out with three replicate dye-swaps, six arrays total. The GFP vs. ERbeta2 comparison was carried out with two replicate dye-swaps, four arrays total.

Dataset Information

Bisphenol A Exposure and Multiple Sclerosis Risk

Publications

Studies in experimental autoimmune encephalomyelitis do not support developmental bisphenol a exposure as an environmental factor in increasing multiple sclerosis risk.

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