Characterisation of gene expression patterns in 22RV1 cells for determination of environmental androgenic/antiandrogenic compounds

Hartel, A.; Didier, Andrea; Pfaffl, Michael W.; Meyer, H. H. D.

doi:10.1016/s0960-0760(03)00033-5

Cited by 27 publications

(13 citation statements)

References 39 publications

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“…Accordingly, we selected a prostate cancer cell-line to further investigate the inhibitory potential of five selected flavonoids. The advantage of using the 22Rv1 prostate cell-line was that unlike the LNCaP, PC-3, and DU145 prostate cells, 22Rv1 cells are derived from a primary prostate carcinoma instead of a metastasis, and the only steroid receptor that they express is the androgen receptor (Hartel et al, 2003). They respond to dihydroxytestosterone, epidermal growth factor, and express prostate specific antigen and, hence, are a good in vitro system to study prostate cancer (Sramkoski et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of human cytochrome CYP1 enzymes by flavonoids of St. John's wort

Chaudhary

Willett

2006

Toxicology

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Section: Discussionmentioning

confidence: 99%

Inhibition of human cytochrome CYP1 enzymes by flavonoids of St. John's wort

Chaudhary

Willett

2006

Toxicology

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“…To confirm the down-regulation of ATBF1 protein expression by estrogen-ER signaling, we transfected the ATBF1 expression plasmid along with ER expression plasmid or vector control into ER and ATBF1 double-negative 22Rv1 cells, which do not express ER (30) and have a frameshift mutation that truncates the majority of ATBF1 protein (8). Transfected cells were then treated with E 2 or alcohol.…”

Section: Knockdown Of Er Down-regulates the Expression Of Atbf1 Atmentioning

confidence: 99%

Estrogen Up-regulates ATBF1 Transcription but Causes Its Protein Degradation in Estrogen Receptor-α-positive Breast Cancer Cells

Dong

Guo

Sun

et al. 2011

Journal of Biological Chemistry

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The proper level of estrogen-estrogen receptor (ER) signaling is important for the maintenance of epithelial homeostasis in the breast. In a previous study we demonstrated that ATBF1, which has been suggested as a tumor suppressor in breast cancer, inhibited estrogen-mediated cell proliferation by selectively competing with AIB1 for binding to the ER. However, the expression of ATBF1 mRNA was shown to positively correlate with ER in breast cancer specimens. We, therefore, examined whether estrogen regulates ATBF1. We demonstrated that estrogen up-regulated the transcription of ATBF1, which was mediated by the direct binding of the ER onto the ATBF1 promoter, and that a half-estrogen-responsive element in the ATBF1 promoter was essential for ER direct binding. Furthermore, we found that estrogen at lower levels increased, but at higher levels decreased the expression of ATBF1 protein, which involved the degradation of ATBF1 protein by the estrogen-responsive proteasome system. ATBF1 protein levels fluctuate with estrogen levels. Although lower levels of estrogen increased ATBF1 protein expression, ATBF1 still inhibited cell proliferation caused by lower levels of estrogen. These findings not only reveal an autoregulatory feedback loop between ATBF1 and estrogen-ER signaling but also suggest that ATBF1 plays a role in both the maintenance of breast epithelial homeostasis and breast tumorigenesis caused by elevated estrogen levels.Extensive studies have established that estrogen is important for the development of the mammary gland and is positively associated with the initiation and development of breast cancer (1). Estrogen exerts its effect through the activation of estrogen receptors, mainly the ␣ subtype (ER␣, 2 or ER hereafter), a member of the nuclear receptor superfamily of transcription factors, which in turn regulates the expression of a variety of genes involved in multiple physiopathological processes including proliferation, differentiation, and apoptosis (2). Tight regulation of estrogen-ER signaling is important for the maintenance of epithelial homeostasis in the breast. In normal mammary epithelial cells, the level and function of ER fluctuates during the menstrual cycle in response to cyclical changes in estrogen (3, 4). ER regulates the expression of a variety of genes through the recruitment of coactivators and corepressors, which are often oncoproteins and tumor suppressors, respectively (5). Estrogen, ER, and coregulators are present in limiting amounts in normal cells. In breast cancer, however, their levels and/or structure are often interrupted, which contributes to the initiation and development of breast cancer (5).The AT-motif binding factor 1 (ATBF1) is a transcription factor composed of 3703 amino acid residues. It was originally identified for its direct binding to and negative regulation of the ␣-fetoprotein gene in a hepatoma cell line (6). In recent studies we identified ATBF1 as a strong candidate for the 16q22 tumor suppressor gene in human cancers, including prostate and breast ...

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“…On the basis of these results, we selected ER-positive cell lines MCF-7 and T-47D and the ER-negative line MDA-MB-231 for further use. We also used the prostate cancer cell line 22Rv1 as an ER and ATBF1 double-negative cell line because it does not express ER (37) and has a frameshift mutation that truncates the majority of ATBF1 protein (21).…”

Section: Atbf1 Protein Expression In Breast Cancer Cell Lines-tomentioning

confidence: 99%

ATBF1 Inhibits Estrogen Receptor (ER) Function by Selectively Competing with AIB1 for Binding to the ER in ER-positive Breast Cancer Cells*

Dong

Sun

Guo

et al. 2010

Journal of Biological Chemistry

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Loss of the q22 band of chromosome 16 is a frequent genetic event in breast cancer, and the candidate tumor suppressor gene, ATBF1, has been implicated in breast cancer by genomic deletion, transcriptional down-regulation, and association with better prognostic parameters. In addition, estrogen receptor (ER)-positive breast cancer expresses a higher level of ATBF1, suggesting a role of ATBF1 in ER-positive breast cancer. In this study, we examined whether and how ATBF1 affects the ER function in breast cancer cells. We found that ATBF1 inhibited ER-mediated gene transcription, cell growth, and proliferation in ER-positive breast cancer cells. In vitro and in vivo immunoprecipitation experiments revealed that ATBF1 interacted physically with the ER and that multiple domains in both ATBF1 and ER proteins mediated the interaction. Furthermore, we demonstrated that ATBF1 inhibited ER function by selectively competing with the steroid receptor coactivator AIB1 but not GRIP1 or SRC1 for binding to the ER. These findings not only support the concept that ATBF1 plays a tumor-suppressive role in breast cancer, they also provide a mechanism for how ATBF1 functions as a tumor suppressor in breast cancer.

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Characterisation of gene expression patterns in 22RV1 cells for determination of environmental androgenic/antiandrogenic compounds

Cited by 27 publications

References 39 publications

Inhibition of human cytochrome CYP1 enzymes by flavonoids of St. John's wort

Inhibition of human cytochrome CYP1 enzymes by flavonoids of St. John's wort

Estrogen Up-regulates ATBF1 Transcription but Causes Its Protein Degradation in Estrogen Receptor-α-positive Breast Cancer Cells

ATBF1 Inhibits Estrogen Receptor (ER) Function by Selectively Competing with AIB1 for Binding to the ER in ER-positive Breast Cancer Cells*

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