ArticleOncogene2001
Mutant BRCA1 genes antagonize phenotype of wild-type BRCA1.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 79 citations in OpenAlex.
- MTAP-ANRIL gene fusion promotes melanoma epithelial-mesenchymal transition-like process by activating the JNK and p38 signaling pathways.Scientific reports · 2023Article
- IL-6/STAT3 signaling in tumor cells restricts the expression of frameshift-derived neoantigens by SMG1 induction.Molecular cancer · 2022Article
- Deciphering the nonsense-mediated mRNA decay pathway to identify cancer cell vulnerabilities for effective cancer therapy.Journal of experimental & clinical cancer research : CR · 2021Review
- Nonsense-mediated RNA decay and its bipolar function in cancer.Molecular cancer · 2021Review
- Review
- Nonsense-mediated mRNA Decay and Cancer.Current opinion in genetics & development · 2018Review
- The retinoblastoma homolog RBR1 mediates localization of the repair protein RAD51 to DNA lesions inThe EMBO journal · 2017Article
- BRCA1-hapoinsufficiency: Unraveling the molecular and cellular basis for tissue-specific cancer.Cell cycle (Georgetown, Tex.) · 2016Review
- MicroRNA-mediated repression of nonsense mRNAs.eLife · 2014Article
- Dissecting disease inheritance modes in a three-dimensional protein network challenges the "guilt-by-association" principle.American journal of human genetics · 2013Article
- Transcriptional regulation of the base excision repair pathway by BRCA1.The Journal of biological chemistry · 2010Article
- BRCA-FA pathway as a target for anti-tumor drugs.Anti-cancer agents in medicinal chemistry · 2008Review
- Review
- BRCA1 and FOXA1 proteins coregulate the expression of the cell cycle-dependent kinase inhibitor p27(Kip1).Oncogene · 2006Article
- BRCA1 and BRCA2 as molecular targets for phytochemicals indole-3-carbinol and genistein in breast and prostate cancer cells.British journal of cancer · 2006Article
- New role for nuclear hormone receptors and coactivators in regulation of BRCA1-mediated DNA repair in breast cancer cell lines.Breast cancer research : BCR · 2006Article
- Article
- Brca1 inactivation induces p27(Kip1)-dependent cell cycle arrest and delayed development in the mouse mammary gland.Oncogene · 2004Article
- The Icelandic founder mutation BRCA2 999del5: analysis of expression.Breast cancer research : BCR · 2004Article
- BRCA1 inhibition of telomerase activity in cultured cells.Molecular and cellular biology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Unregulated expression of wild-type BRCA1 (wtBRCA1) confers an altered phenotype in cultured human prostate cancer cells, characterized by chemosensitivity, susceptibility to apoptosis, decreased DNA repair activity, and alterations of key cell regulatory proteins. We now report that the expression of truncated or mutant full-length BRCA1 genes can abrogate certain phenotypic characteristics and/or confer the opposite phenotype to the wild-type BRCA1 gene. In particular, several carboxyl-terminal truncated BRCA1 proteins conferred chemoresistance, decreased susceptibility to apoptosis, and decreased ability to suppress in vivo tumor growth. These truncated BRCA1 proteins also blocked the ability of ectopically expressed wtBRCA1 to induce chemosensitivity and to inhibit estrogen receptor transcriptional activity. Studies using epitope-tagged truncated proteins confirmed their expression, nuclear localization, and functionality. On the other hand, in cells with no endogenous wild-type BRCA1 (HCC1937 human breast cancer cells), the wtBRCA1 gene enhanced cellular DNA repair activity and rendered the cells resistant to DNA damage; while truncated BRCA1 proteins blocked the wtBRCA1-induced chemoresistance. Our findings suggest that truncated BRCA1 proteins can inhibit the function of wild-type BRCA1. They raise the possibility that some inherited BRCA1 mutations may actively promote oncogenesis by blocking the function of the remaining wild-type BRCA1 allele, although this hypothesis remains to be proved.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.