ArticleOncogene2008
BRE is an antiapoptotic protein in vivo and overexpressed in human hepatocellular carcinoma.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
- SAMD13 serves as a useful prognostic biomarker for hepatocellular carcinoma.European journal of medical research · 2023Article
- PPDPF Promotes the Progression and acts as an Antiapoptotic Protein in Non-Small Cell Lung Cancer.International journal of biological sciences · 2022Article
- Babam2 negatively regulates osteoclastogenesis by interacting with Hey1 to inhibit Nfatc1 transcription.International journal of biological sciences · 2022Article
- SMAD4-induced knockdown of the antisense long noncoding RNA BRE-AS contributes to granulosa cell apoptosis.Molecular therapy. Nucleic acids · 2021Article
- Babam2 Regulates Cell Cycle Progression and Pluripotency in Mouse Embryonic Stem Cells as Revealed by Induced DNA Damage.Biomedicines · 2020Article
- BRE Promotes Esophageal Squamous Cell Carcinoma Growth by Activating AKT Signaling.Frontiers in oncology · 2020Article
- C-terminal BRE overexpression in 11q23-rearranged and t(8;16) acute myeloid leukemia is caused by intragenic transcription initiation.Leukemia · 2018Article
- BRE/BRCC45 regulates CDC25A stability by recruiting USP7 in response to DNA damage.Nature communications · 2018Article
- Resistance a major hindrance to chemotherapy in hepatocellular carcinoma: an insight.Cancer cell international · 2018Review
- Macrolide antibiotics differentially influence human HepG2 cytotoxicity and modulate intrinsic/extrinsic apoptotic pathways in rat hepatocellular carcinoma model.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Over-expression of the long non-coding RNA HOTTIP inhibits glioma cell growth by BRE.Journal of experimental & clinical cancer research : CR · 2016Article
- BRE plays an essential role in preventing replicative and DNA damage-induced premature senescence.Scientific reports · 2016Article
- Anti-apoptotic brain and reproductive organ-expressed proteins enhance cisplatin resistance in lung cancer cells via the protein kinase B signaling pathway.Thoracic cancer · 2016Article
- BRE facilitates skeletal muscle regeneration by promoting satellite cell motility and differentiation.Biology open · 2016Article
- Apoptosis in liver carcinogenesis and chemotherapy.Hepatic oncology · 2015Review
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- Mechanisms and biomarkers of apoptosis in liver disease and fibrosis.International journal of hepatology · 2012Article
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- High BRE expression in pediatric MLL-rearranged AML is associated with favorable outcome.Leukemia · 2010Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRE binds to the cytoplasmic domains of tumor necrosis factor receptor-1 and Fas, and in cell lines can attenuate death receptor-initiated apoptosis by inhibiting t-BID-induced activation of the mitochondrial apoptotic pathway. Overexpression of BRE by transfection can also attenuate intrinsic apoptosis and promote growth of the transfected Lewis lung carcinoma line in mice. There is, however, a complete lack of in vivo data about the protein. Here, we report that by using our BRE-specific monoclonal antibody on the immunohistochemistry of 123 specimens of human hepatocellular carcinoma (HCC), significant differences in BRE expression levels between the paired tumoral and non-tumoral regions (P<2.2e-16) were found. Marked overexpression of BRE was detected in majority of the tumors, whereas most non-tumoral regions expressed the same low level of the protein as in normal livers. To investigate whether BRE overexpression could promote cell survival in vivo, liver-specific transgenic BRE mice were generated and found to be significantly resistant to Fas-mediated lethal hepatic apoptosis. The transgenic model also revealed post-transcriptional regulation of Bre level in the liver, which was not observed in HCC and non-HCC cell lines. Indeed, all cell lines analysed express high levels of BRE. In conclusion, BRE is antiapoptotic in vivo, and may promote tumorigenesis when overexpressed.
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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.