scholarly journals Establishment of a C3Hf Mammary Tumor Cell Line Expressing Endogenous Mouse Mammary Tumor Virus: Antigenic and Genetic Relationships of This Virus with Highly Oncogenic Mouse Mammary Tumor Viruses

1979 ◽  
Vol 32 (3) ◽  
pp. 852-859 ◽  
Author(s):  
Larry O. Arthur ◽  
Gerald G. Lovinger ◽  
Gerald Schochetman
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Genetic Relationships ◽  
Tumor Cell Line ◽  
Mammary Tumor Cell ◽  
Mammary Tumor Virus ◽  
Mammary Tumor Cell Line ◽  
Tumor Viruses ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

scholarly journals Mutations in the hormone regulatory element of mouse mammary tumor virus differentially affect the response to progestins, androgens, and glucocorticoids.

1989 ◽  
Vol 9 (9) ◽  
pp. 3999-4008 ◽  
Author(s):  
P L Gowland ◽  
E Buetti
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Regulatory Element ◽  
Tumor Cell Line ◽  
Proximal Region ◽  
Mammary Tumor Cell ◽  
Mammary Tumor Virus ◽  
Mammary Tumor Cell Line ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Transcription of the mouse mammary tumor virus DNA is known to be induced by several steroid hormones. Using chimeric MMTV plasmids containing mutations within the hormone regulatory element, we have previously studied the regions required for the glucocorticoid response in mouse fibroblasts. Here we report the characterization of elements essential for the stimulation by progestins and androgens as compared with glucocorticoids. The same set of mutant plasmids was transfected into the human mammary tumor cell line T47D, and the specific transcripts were analyzed by an S1 nuclease protection assay. Androgen-mediated stimulation, although weak, showed an extended sensitivity to mutations, with a slight preference for the proximal region. The results with progestin suggest that sequences within all the described sites protected by the receptor in vitro are required and that the promoter-proximal region (-128 to -78 from the RNA start site) is more important than the distal one (-190 to -160). Moreover, a binding site for nuclear factor I was not required for the progestin response, whereas it was required for glucocorticoids. Thus, the various steroid receptors play a role in the differential regulation of mouse mammary tumor virus transcription by recognizing distinct sequence differences in the hormone regulatory element and interacting with different factors bound to the promoter.

scholarly journals Mutations in the hormone regulatory element of mouse mammary tumor virus differentially affect the response to progestins, androgens, and glucocorticoids

1989 ◽  
Vol 9 (9) ◽  
pp. 3999-4008
Author(s):  
P L Gowland ◽  
E Buetti
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Regulatory Element ◽  
Tumor Cell Line ◽  
Proximal Region ◽  
Mammary Tumor Cell ◽  
Mammary Tumor Virus ◽  
Mammary Tumor Cell Line ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Transcription of the mouse mammary tumor virus DNA is known to be induced by several steroid hormones. Using chimeric MMTV plasmids containing mutations within the hormone regulatory element, we have previously studied the regions required for the glucocorticoid response in mouse fibroblasts. Here we report the characterization of elements essential for the stimulation by progestins and androgens as compared with glucocorticoids. The same set of mutant plasmids was transfected into the human mammary tumor cell line T47D, and the specific transcripts were analyzed by an S1 nuclease protection assay. Androgen-mediated stimulation, although weak, showed an extended sensitivity to mutations, with a slight preference for the proximal region. The results with progestin suggest that sequences within all the described sites protected by the receptor in vitro are required and that the promoter-proximal region (-128 to -78 from the RNA start site) is more important than the distal one (-190 to -160). Moreover, a binding site for nuclear factor I was not required for the progestin response, whereas it was required for glucocorticoids. Thus, the various steroid receptors play a role in the differential regulation of mouse mammary tumor virus transcription by recognizing distinct sequence differences in the hormone regulatory element and interacting with different factors bound to the promoter.

Androgen regulation by the long terminal repeat of mouse mammary tumor virus

1986 ◽  
Vol 6 (8) ◽  
pp. 2847-2854
Author(s):  
P Darbre ◽  
M Page ◽  
R J King
Keyword(s):  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Terminal Repeat ◽  
Regulatory Sequences ◽  
Mammary Tumor Cell ◽  
Mammary Tumor Virus ◽  
Mammary Tumor Cell Line ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Mouse mammary tumor virus (MMTV) has long been implicated in mouse mammary carcinogenesis, and it is now well established that the long terminal repeat (LTR) contains regulatory sequences responsible for glucocorticoid-mediated induction of viral RNA. However, we have demonstrated previously that androgens as well as glucocorticoids can regulate MMTV RNA in the S115 mouse mammary tumor cell line. To determine if androgens act directly on the LTR in these cells, plasmids were constructed with the MMTV LTR joined to the coding sequences of genes not normally expressed in the cells. Following transfection of these chimeric genes into S115 cells, we show that the expression of the genes is regulated by both androgens and glucocorticoids. Furthermore, hormonal regulation is also conferred by the LTR on the neighboring guanine phosphoribosyltransferase (gpt) gene. Thus, androgens can act on the LTR of MMTV when the appropriate receptors are present in the cells, and this interaction can influence the expression of additional adjacent genes.

scholarly journals Androgen regulation by the long terminal repeat of mouse mammary tumor virus.

1986 ◽  
Vol 6 (8) ◽  
pp. 2847-2854 ◽  
Author(s):  
P Darbre ◽  
M Page ◽  
R J King
Keyword(s):  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Terminal Repeat ◽  
Regulatory Sequences ◽  
Mammary Tumor Cell ◽  
Mammary Tumor Virus ◽  
Mammary Tumor Cell Line ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Mouse mammary tumor virus (MMTV) has long been implicated in mouse mammary carcinogenesis, and it is now well established that the long terminal repeat (LTR) contains regulatory sequences responsible for glucocorticoid-mediated induction of viral RNA. However, we have demonstrated previously that androgens as well as glucocorticoids can regulate MMTV RNA in the S115 mouse mammary tumor cell line. To determine if androgens act directly on the LTR in these cells, plasmids were constructed with the MMTV LTR joined to the coding sequences of genes not normally expressed in the cells. Following transfection of these chimeric genes into S115 cells, we show that the expression of the genes is regulated by both androgens and glucocorticoids. Furthermore, hormonal regulation is also conferred by the LTR on the neighboring guanine phosphoribosyltransferase (gpt) gene. Thus, androgens can act on the LTR of MMTV when the appropriate receptors are present in the cells, and this interaction can influence the expression of additional adjacent genes.

scholarly journals BALB/Mtv-Null Mice Responding to Strong Mouse Mammary Tumor Virus Superantigens Restrict Mammary Tumorigenesis

2008 ◽  
Vol 83 (1) ◽  
pp. 484-488 ◽  
Author(s):  
Sanchita Bhadra ◽  
Mary M. Lozano ◽  
Jaquelin P. Dudley
Keyword(s):  
Mammary Gland ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumorigenesis ◽  
Congenic Mouse ◽  
Tumor Induction ◽  
Mammary Tumor Virus ◽  
Tumor Viruses ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

ABSTRACT The absence of endogenous mouse mammary tumor viruses (MMTVs) in the congenic mouse strain, BALB/Mtv-null, restricts the early steps of exogenous C3H MMTV infection, preventing the superantigen (Sag) response and mammary tumorigenesis. Here we demonstrate that BALB/Mtv-null mice also resist tumor induction by FM MMTV, which encodes a stronger Sag compared to C3H MMTV. In contrast to infections with C3H MMTV, Mtv-null mice show FM-MMTV Sag-specific responses comparable to those observed in susceptible BALB/c mice. Neither virus shows significant replication in the spleen or mammary gland. Thus, Mtv-null mice restrict MMTV replication and mammary tumorigenesis even after a robust Sag response.

Electron Microscopy of the Nucleic Acid of Mouse Mammary Tumor Virus

1968 ◽  
Vol 26 ◽  
pp. 22-23
Author(s):  
N. H. Sarkar ◽  
Dan H. Moore
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Ammonium Acetate ◽  
Dry Weight ◽  
Mouse Tumor ◽  
Mammary Tumor Virus ◽  
Rna Molecules ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
The Subject

Mouse mammary tumor virus (MTV) is believed to contain about 0.8% single stranded ribonucleic acid (RNA). This value of RNA content was estimated on a dry weight basis. The subject of this report is an attempt to visualize the RNA molecules of MTV particles.MTV particles were isolated from RIII mouse (tumor incidence approximately 80%) milk according to the method described by Lyons and Moore. Purified virions from 5 ml of milk were finally suspended in 0.2 ml of PBS, pH 7.4 and was mixed with an equal volume of pronase (5 mg/ml). This mixture was incubated at 37°C for an hour. RNA was extracted three times using freshly prepared cold phenol. It was then treated three times with cold ethyl ether to remove any trace of phenol. The RNA thus extracted was divided into two parts. One part was diluted four fold with 8M urea to avoid aggregation of the molecules. The other part was left untreated. Both samples were then mixed with an equal volume of 1M ammonium acetate, adjusted to pH 8.0 with NH3 containing chymotrypsin at a concentration of 0.01%.

Sign in / Sign up

Export Citation Format

Share Document