Oestrogen enhances the responsiveness of the MMTV-LTR to glucocorticoid in ZR-75-1 human breast cancer cells

Bansal, Gurpal S.; Latchman, David S.

doi:10.1016/0022-4731(90)90080-c

Journal of Steroid Biochemistry

1990

DOI: 10.1016/0022-4731(90)90080-c

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Oestrogen enhances the responsiveness of the MMTV-LTR to glucocorticoid in ZR-75-1 human breast cancer cells

Gurpal S. Bansal

David S. Latchman

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Cited by 3 publications

References 23 publications

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Modulation of Androgen Receptor Transcriptional Activity by the Estrogen Receptor

KUMAR,

LEO,

TINDALL

1994

Journal of Andrology

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Estrogen/androgen receptor interactions in naturally occurring physiological systems and the effect of their respective steroid hormones on transcriptional activity remain undefined. In an attempt to delineate further the nature of the interaction between these two steroid hormone receptors we have examined the effect of cotransfection of androgen (AR) and estrogen receptor (ER) cDNAs on the expression of the mouse mammary tumor virus long terminal repeat region (MMTV‐LTR) linked to the chloramphenicol‐acetyl‐transferase (CAT) reporter gene. In QT6 cells, which contain neither AR nor ER, cotransfection of AR cDNA with the MMTV‐LTR‐CAT reporter, resulted in transactivation only in the presence of dihydrotestosterone (DHT). Treatment with 10−8 M each of estradiol‐17β (E2), dexamethasone, or progesterone did not enhance CAT activity, whereas treatment with the androgens DHT and mibolerone resulted in 87% and 89% CAT activity. Transfection of increasing concentrations of ER cDNA in the presence of 100 ng of AR cDNA and 10−8 M each of DHT and E2 showed a dose‐dependent decrease in CAT activity as compared to the response with DHT alone. Cotransfection of AR and ER cDNA in the presence of 10−8 M DHT and increasing concentrations of E2 resulted in a dose‐dependent decrease in CAT activity. When cells were treated with increasing concentrations of DHT with 10−8 M E2 no significant increase in CAT activity was observed. In GC cells, which contain endogenous ER but no AR, cotransfection of AR cDNA and treatment with E2 and DHT, also reduced DHT‐induced CAT activity. Thus, we conclude that the E2 ER complex is capable of inhibiting transcriptional activity of the AR.

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Modulation of Androgen Receptor Transcriptional Activity by the Estrogen Receptor

KUMAR,

LEO,

TINDALL

1994

Journal of Andrology

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Overexpression of estrogen receptor in HTB 96 human osteosarcoma cells results in estrogen-induced growth inhibition and receptor cross talk

Watts

King

1994

Journal of Bone and Mineral Research

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Estrogenic effects on the proliferation and differentiated cellular functions of bone cells have been described in vivo and in vitro. In particular, stimulatory effects on the growth rate of osteoblasts have been observed, although these are generally small. In an attempt to produce a more sensitive model for the study of estrogen action in bone, HTB 96 human osteoblast-like osteosarcoma cells, which lack endogenous estrogen receptor (ER), were stably transfected with an expression vector coding for the human ER gene. Several HTB 96 sublines expressing ER protein, detected by ligand binding and immunoassay, were isolated. The ability of 17 beta-estradiol (E2) to induce chloramphenicol acetyltransferase (CAT) activity from a cotransfected reporter vector containing the CAT gene linked to the Xenopus vitellogenin A2 gene estrogen response element demonstrated that the expressed ER was functional. ER continued to be expressed over a 30 week culture period. E2 but not other steroids significantly reduced growth rates and produced an altered morphology in HTB 96 sublines expressing higher levels of ER. The antiestrogen 4-hydroxytamoxifen partially reversed the E2 effect on growth rate. Transient transfection of cells expressing ER with a vector containing the CAT gene linked to the mouse mammary tumor virus long terminal repeat sequence, which contains response elements for the glucocorticoid receptor but not the ER, showed that E2 was able to inhibit CAT induction by dexamethasone. This result suggest that in ER-transfected HTB 9 cells the effects of E2 may result not from direct activation of endogenous genes but instead by transcriptional interference.(ABSTRACT TRUNCATED AT 250 WORDS)

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The Porcine Endogenous Retrovirus Long Terminal Repeat Contains a Single Nucleotide Polymorphism That Confers Distinct Differences in Estrogen Receptor Binding Affinity between PERV A and PERV B/C Subtypes

Quinn

Langford

2001

Virology

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Porcine endogenous retroviruses (PERV) have been shown to have zoonotic potential, both in vitro and in vivo. Once integrated into the host cell genome activation of the proviral genes is ultimately dependent upon transactivation of the long terminal repeat (LTR). Currently there is no direct evidence of host cell transcription factors interacting with PERV LTRs. Using comparative genomics we discovered a potentially functional single nucleotide polymorphism (SNP) within the U5 region downstream of the TATA box in the PERV LTR that distinguishes PERV A from PERV B and PERV C subtypes. We demonstrated that the SNP occurs within a potential hormone-responsive region where it has a profound effect, not only upon estrogen receptor binding but also upon the binding of other transcription factors at this site. These results suggest that differences in transcriptional regulation between PERV subtypes are subtle and, as for other retroviruses, transcription can be mediated by steroid hormone receptors.

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Oestrogen enhances the responsiveness of the MMTV-LTR to glucocorticoid in ZR-75-1 human breast cancer cells

Cited by 3 publications

References 23 publications

Modulation of Androgen Receptor Transcriptional Activity by the Estrogen Receptor

Modulation of Androgen Receptor Transcriptional Activity by the Estrogen Receptor

Overexpression of estrogen receptor in HTB 96 human osteosarcoma cells results in estrogen-induced growth inhibition and receptor cross talk

The Porcine Endogenous Retrovirus Long Terminal Repeat Contains a Single Nucleotide Polymorphism That Confers Distinct Differences in Estrogen Receptor Binding Affinity between PERV A and PERV B/C Subtypes

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