ArticleMolecular and cellular biology2011
A novel transcription complex that selectively modulates apoptosis of breast cancer cells through regulation of FASTKD2.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed, 69 citations in OpenAlex.
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- Cardiac Myocyte-Specific Overexpression of FASTKD1 Prevents Ventricular Rupture After Myocardial Infarction.Journal of the American Heart Association · 2023Article
- The mitochondrial RNA granule modulates manganese-dependent cell toxicity.Molecular biology of the cell · 2022Article
- FASTK family of genes linked to cancer.Bioinformation · 2022Article
- Integrated profiling identifies ITGB3BP as prognostic biomarker for hepatocellular carcinoma.Bosnian journal of basic medical sciences · 2021Article
- Identification and Functional Characterization of a Novel Androgen Receptor Coregulator, EAP1.Journal of the Endocrine Society · 2021Article
- Systematic Analysis of FASTK Gene Family Alterations in Cancer.International journal of molecular sciences · 2021Article
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- Irf2bp2a regulates terminal granulopoiesis through proteasomal degradation of Gfi1aa in zebrafish.PLoS genetics · 2021Article
- Antisense Oligonucleotide-Based Therapeutic against Menin for Triple-Negative Breast Cancer Treatment.Biomedicines · 2021Article
- Transient deSUMOylation of IRF2BP proteins controls early transcription in EGFR signaling.EMBO reports · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We previously reported that expression of NRIF3 (nuclear receptor interacting factor-3) rapidly and selectively leads to apoptosis of breast cancer cells. DIF-1 (also known as interferon regulatory factor-2 binding protein 2 [IRF-2BP2]), the cellular target of NRIF3, was identified as a transcriptional repressor, and DIF-1 knockdown leads to apoptosis of breast cancer cells but not other cell types. Here, we identify IRF-2BP1 and EAP1 (enhanced at puberty 1) as important components of the DIF-1 complex mediating both complex stability and transcriptional repression. This interaction of DIF-1, IRF-2BP1, and EAP1 occurs through the conserved C4 zinc fingers of these proteins. Microarray studies were carried out in breast cancer cell lines engineered to conditionally and rapidly increase the levels of the death domain (DD1) region of NRIF3. The DIF-1 complex was found to repress FASTKD2, a putative proapoptotic gene, in breast cancer cells and to bind to the FASTKD2 gene by chromatin immunoprecipitation. FASTKD2 knockdown prevents apoptosis of breast cancer cells from NRIF3 expression or DIF-1 knockdown, while expression of FASTKD2 leads to apoptosis of both breast and nonbreast cancer cells. Thus, regulation of FASTKD2 by NRIF3 and the DIF-1 complex acts as a novel death switch that selectively modulates apoptosis in breast cancer.
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