ArticleMolecular cancer research : MCR2018
BRCA1 through Its E3 Ligase Activity Regulates the Transcription Factor Oct1 and Carbohydrate Metabolism.
Article in Molecular cancer research : MCR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Suppression of OCT-1 in Metastatic Breast Cancer Cells Reduces Tumor Metastatic Potential, Hypoxia Resistance, and Drug Resistance.Life (Basel, Switzerland) · 2022Article
- The BRCA1/BARD1 ubiquitin ligase and its substrates.The Biochemical journal · 2021Review
- Octamer transcription factor-1 induces the Warburg effect via up-regulation of hexokinase 2 in non-small cell lung cancer.Molecular and cellular biochemistry · 2021Article
- New genetic prognostic biomarkers in primary central nervous system lymphoma (PCNSL).Brain and behavior · 2021Article
- BRCA1/BARD1 site-specific ubiquitylation of nucleosomal H2A is directed by BARD1.Nature structural & molecular biology · 2021Article
- Plasma Metabolome Signature Indicative ofFrontiers in oncology · 2021Article
- Recent Discoveries in the Androgen Receptor Pathway in Castration-Resistant Prostate Cancer.Frontiers in oncology · 2020Review
- PFKP is transcriptionally repressed by BRCA1/ZBRK1 and predicts prognosis in breast cancer.PloS one · 2020Article
- Transcription factor Oct1 protects against hematopoietic stress and promotes acute myeloid leukemia.Experimental hematology · 2019Article
- Oct1/Pou2f1 is selectively required for colon regeneration and regulates colon malignancy.PLoS genetics · 2019Article
- Preventing BRCA1/ZBRK1 repressor complex binding to the GOT2 promoter results in accelerated aspartate biosynthesis and promotion of cell proliferation.Molecular oncology · 2019Article
- Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The tumor suppressor BRCA1 regulates the DNA damage response (DDR) and other processes that remain incompletely defined. Among these, BRCA1 heterodimerizes with BARD1 to ubiquitylate targets via its N-terminal E3 ligase activity. Here, it is demonstrated that BRCA1 promotes oxidative metabolism by degrading Oct1 (POU2F1), a transcription factor with proglycolytic and tumorigenic effects. BRCA1 E3 ubiquitin ligase mutation skews cells toward a glycolytic metabolic profile while elevating Oct1 protein. CRISPR-mediated Oct1 deletion reverts the glycolytic phenotype. RNA sequencing (RNAseq) confirms deregulation of metabolic genes downstream of Oct1. BRCA1 mediates Oct1 ubiquitylation and degradation, and mutation of two ubiquitylated Oct1 lysines insulates the protein against BRCA1-mediated destabilization. Oct1 deletion in MCF-7 breast cancer cells does not perturb growth in standard culture, but inhibits growth in soft agar and xenograft assays. In primary breast cancer clinical specimens, Oct1 protein levels correlate positively with tumor aggressiveness and inversely with BRCA1. These results identify BRCA1 as an Oct1 ubiquitin ligase that catalyzes Oct1 degradation to promote oxidative metabolism and restrict tumorigenicity.
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