Frequent activation of CArG binding factor-A expression and binding in N-methyl-N-nitrosourea-induced rat mammary carcinomas
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/262191
- author
- Mikheev, A M ; Inoue, A ; Jing, L C ; Mikheeva, S A ; Li, V ; Leanderson, Tomas LU and Zarbl, H
- organization
- publishing date
- 2004
- 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
- 2016-04-01 16:49:18
- date last changed
- 2022-01-28 22:23:13
@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}},
keywords = {{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}},
doi = {{10.1007/s10549-004-1280-5}},
volume = {{88}},
year = {{2004}},
}