Expression of the BRCA1-interacting protein Brip1/BACH1/FANCJ is driven by E2F and correlates with human breast cancer malignancy
Open accessAbstract
Mutations in the BRCA1-interacting DEAH helicase Brip1 confer an increased risk of breast cancer. In the present study we aimed to unravel the transcriptional control of Brip1 and to determine its expression levels in a set of 101 primary invasive breast carcinomas. Transcription of Brip1 was found to be cell growth-related and controlled by the E2F/retinoblastoma (Rb) pathway through a conserved E2F-responsive site. Repression of Brip1 expression by the cell growth-inhibiting compound 1alpha,25-dihydroxyvitamin D3 depended on this same E2F-responsive site. In spite of its role as a tumor suppressor, both quantitative reverse transcriptase-PCR analyses and immunohistochemical stainings showed significantly elevated Brip1 expression levels in grade 3 tumors as compared to grade 1 or 2 carcinomas. Furthermore, increased Brip1 transcript levels were found in tumors with an estrogen receptor-negative, progesterone receptor-negative or HER-2-positive status. In conclusion, these data show that Brip1 is a genuine target gene for the E2F/Rb pathway and that elevated expression levels of Brip1 are detected in primary invasive breast carcinomas with unfavorable characteristics.
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FANCJ transcription is cell growth-related and controlled by tumor suppressors of the E2F-retinoblastoma pathway.
“It remains to be determined whether cancer is associated with changes in FANCJ transcription, which is cell growth-related and controlled by tumor suppressors of the E2F–retinoblastoma pathway [67].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [67]
Elevated FANCJ expression levels were detected in grade 3 invasive breast tumors and correlated with poor prognosis.
“In support of this possibility, elevated FANCJ expression levels were detected in grade 3 invasive breast tumors and correlated with poor prognosis [67].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [67]
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- Authors
- Eelen, G., Vanden Bempt, I., Verlinden, L., Drijkoningen, M., Smeets, A., Neven, P., Christiaens, M. R., Marchal, K., Bouillon, R., & Verstuyf, A.
- Affiliations
- KU Leuven (BE)
- Universitair Ziekenhuis Leuven (BE)
- Corresponding author
- Verstuyf, A
- Venue
- Oncogene
- Published
- 2008-03-17
- Volume
- 27
- Issue
- 30
- Pages
- 4233-4241
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W1969171797
- Cited by
- 41
- References
- 33
- Citations by year
- 2024: 1 · 2022: 3 · 2021: 4 · 2020: 3 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 1 · 2015: 1 · 2013: 3 · 2012: 3
- FWCI
- 2.81
- Type
- journal article
- Language
- en
- Open access
- green
- lirias.kuleuven.be
- Licence
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Lirias (submittedVersion, other-oa)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Funders
- Fonds Wetenschappelijk Onderzoek
- KU Leuven
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- BRIP1, BACH1, FANCJ, transcriptional regulation, breast cancer, tumor grade, estrogen receptor-negative, progesterone receptor-negative, HER2-positive, 1,25-dihydroxyvitamin D3, tumor suppressor
- MeSH terms
- Animals, Base Sequence, Binding Sites, Breast Neoplasms, Carcinoma, DNA-Binding Proteins, Female, Humans, Molecular Sequence Data, Neoplasm Invasiveness, Sequence Homology, Nucleic Acid, Transcription, Genetic, Tumor Cells, Cultured, Gene Expression Regulation, Neoplastic, Conserved Sequence, RNA Helicases, E2F Transcription Factors, Basic-Leucine Zipper Transcription Factors, Mice, Fanconi Anemia Complementation Group Proteins
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