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Frequent activation of CArG binding factor-A expression and binding in N-methyl-N-nitrosourea-induced rat mammary carcinomas

Mikheev, A M; Inoue, A; Jing, L C; Mikheeva, S A; Li, V; Leanderson, Tomas LU and Zarbl, H (2004) In Breast Cancer Research and Treatment 88(1). p.95-102
Abstract
We previously identified a positive transcriptional element identical to human Ha-ras response element ( HRE) within the promoter of the rat Ha-ras gene. We further identified CArG binding factor A ( CBF-A), a member of heterogeneous nuclear ribonuclear protein ( hnRNP) gene family, as a trans-acting factor that binds the HRE sequence with high affinity in rat mammary carcinoma cells. To determine if activation of CBF-A plays a role in tumor development in vivo, we investigated CBF-A expression and binding activity in rat mammary tumors induced by N-methyl-N-nitrosourea. We found that -82% of tumors expressed CBFA at levels that were 3-20 fold higher than detected in normal mammary gland. Moreover, elevated CBF-A protein levels were... (More)
We previously identified a positive transcriptional element identical to human Ha-ras response element ( HRE) within the promoter of the rat Ha-ras gene. We further identified CArG binding factor A ( CBF-A), a member of heterogeneous nuclear ribonuclear protein ( hnRNP) gene family, as a trans-acting factor that binds the HRE sequence with high affinity in rat mammary carcinoma cells. To determine if activation of CBF-A plays a role in tumor development in vivo, we investigated CBF-A expression and binding activity in rat mammary tumors induced by N-methyl-N-nitrosourea. We found that -82% of tumors expressed CBFA at levels that were 3-20 fold higher than detected in normal mammary gland. Moreover, elevated CBF-A protein levels were invariably associated with increased binding activity to the HRE. CBF-A mRNA levels in tumors were on average elevated only two fold as compared to normal mammary gland, indicating that increased CBF-A protein levels in tumors resulted from both translational and/or post-translational regulation. The level of CBF-A expression in mammary tumors was independent of Ha-ras mutational status. Together, these findings indicated that deregulation of CBF-A contributes to mammary carcinogenesis via a mechanism that is distinct from its hnRNP functions in binding and post-transcriptional regulation of RNA. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
mammary tumor, CArG binding factor A, heterogeneous nuclear ribonuclear protein, N-methyl-N-nitrosourea
in
Breast Cancer Research and Treatment
volume
88
issue
1
pages
95 - 102
publisher
Springer
external identifiers
  • wos:000225022300011
  • pmid:15538050
  • scopus:8744220668
ISSN
1573-7217
DOI
10.1007/s10549-004-1280-5
language
English
LU publication?
yes
id
f3ca1c9e-515d-4f48-b2e8-f7253967b408 (old id 262191)
date added to LUP
2007-10-26 16:34:55
date last changed
2017-01-01 07:16:11
@article{f3ca1c9e-515d-4f48-b2e8-f7253967b408,
  abstract     = {We previously identified a positive transcriptional element identical to human Ha-ras response element ( HRE) within the promoter of the rat Ha-ras gene. We further identified CArG binding factor A ( CBF-A), a member of heterogeneous nuclear ribonuclear protein ( hnRNP) gene family, as a trans-acting factor that binds the HRE sequence with high affinity in rat mammary carcinoma cells. To determine if activation of CBF-A plays a role in tumor development in vivo, we investigated CBF-A expression and binding activity in rat mammary tumors induced by N-methyl-N-nitrosourea. We found that -82% of tumors expressed CBFA at levels that were 3-20 fold higher than detected in normal mammary gland. Moreover, elevated CBF-A protein levels were invariably associated with increased binding activity to the HRE. CBF-A mRNA levels in tumors were on average elevated only two fold as compared to normal mammary gland, indicating that increased CBF-A protein levels in tumors resulted from both translational and/or post-translational regulation. The level of CBF-A expression in mammary tumors was independent of Ha-ras mutational status. Together, these findings indicated that deregulation of CBF-A contributes to mammary carcinogenesis via a mechanism that is distinct from its hnRNP functions in binding and post-transcriptional regulation of RNA.},
  author       = {Mikheev, A M and Inoue, A and Jing, L C and Mikheeva, S A and Li, V and Leanderson, Tomas and Zarbl, H},
  issn         = {1573-7217},
  keyword      = {mammary tumor,CArG binding factor A,heterogeneous nuclear ribonuclear protein,N-methyl-N-nitrosourea},
  language     = {eng},
  number       = {1},
  pages        = {95--102},
  publisher    = {Springer},
  series       = {Breast Cancer Research and Treatment},
  title        = {Frequent activation of CArG binding factor-A expression and binding in N-methyl-N-nitrosourea-induced rat mammary carcinomas},
  url          = {http://dx.doi.org/10.1007/s10549-004-1280-5},
  volume       = {88},
  year         = {2004},
}