ArticleProceedings of the National Academy of Sciences of the United States of America2007
Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 82 papers.
What it found
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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.
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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.
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Who cites it
82 citing papers in PubMed, 127 citations in OpenAlex.
- Contribution of MylA in Conidiogenesis, Conidia Germination, and beta-Glucan Biosynthesis inJournal of microbiology and biotechnology · 2026Article
- Distal enhancer RNAs regulate alternative promoter usage of MYB and drug resistance in human leukemia cells.Leukemia · 2026Article
- MUC1-C dependency in drug resistant HR+/HER2- breast cancer identifies a new target for antibody-drug conjugate treatment.NPJ breast cancer · 2025Article
- miRNA-dependent resistance mechanisms to anti-hormonal therapies in estrogen receptor-positive breast cancer patients.Molecular therapy. Oncology · 2025Review
- Artificial intelligence-assisted RNA-binding protein signature for prognostic stratification and therapeutic guidance in breast cancer.Frontiers in immunology · 2025Article
- Discovery of therapeutic targets in cancer using chromatin accessibility and transcriptomic data.Cell systems · 2024Article
- The MYB-like protein MylA contributes to conidiogenesis and conidial germination in Aspergillus nidulans.Communications biology · 2024Article
- Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024Review
- Article
- From modulation of cellular plasticity to potentiation of therapeutic resistance: new and emerging roles of MYB transcription factors in human malignancies.Cancer metastasis reviews · 2024Review
- Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- CRISPR/Cas9 screen uncovers functional translation of cryptic lncRNA-encoded open reading frames in human cancer.The Journal of clinical investigation · 2023Article
- Cistrome Explorer: an interactive visual analysis tool for large-scale epigenomic data.Bioinformatics (Oxford, England) · 2023Article
- Multimodal 4-arylchromene derivatives with microtubule-destabilizing, anti-angiogenic, and MYB-inhibitory activities.Cancer drug resistance (Alhambra, Calif.) · 2023Article
- Protein kinase C targeting of luminal (T-47D), luminal/HER2-positive (BT474), and triple negative (HCC1806) breast cancer cells in-vitro with AEB071 (Sotrastaurin) is efficient but mediated by subtype specific molecular effects.Archives of gynecology and obstetrics · 2022Article
- Natural Products with Antitumor Potential Targeting the MYB-C/EBPβ-p300 Transcription Module.Molecules (Basel, Switzerland) · 2022Review
- Rational design of a helical peptide inhibitor targeting c-Myb-KIX interaction.Scientific reports · 2022Article
- Bcr-TMP, a Novel Nanomolar-Active Compound That Exhibits Both MYB- and Microtubule-Inhibitory Activity.Cancers · 2021Article
- Review
- Estrogen Receptor-α Suppresses Liver Carcinogenesis and Establishes Sex-Specific Gene Expression.Cancers · 2021Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
MYB (the human ortholog of c-myb) is expressed in a high proportion of human breast tumors, and that expression correlates strongly with estrogen receptor (ER) positivity. This may reflect the fact that MYB is a target of estrogen/ER signaling. Because in many cases MYB expression appears to be regulated by transcriptional attenuation or pausing in the first intron, we first investigated whether this mechanism was involved in estrogen/ER modulation of MYB. We found that this was the case and that estrogen acted directly to relieve attenuation due to sequences within the first intron, specifically, a region potentially capable of forming a stem-loop structure in the transcript and an adjacent poly(dT) tract. Secondly, given the involvement of MYB in hematopoietic and colon tumors, we also asked whether MYB was required for the proliferation of breast cancer cells. We found that proliferation of ER(+) but not ER(-) breast cancer cell lines was inhibited when MYB expression was suppressed by using either antisense oligonucleotides or RNA interference. Our results show that MYB is an effector of estrogen/ER signaling and provide demonstration of a functional role of MYB in breast cancer.
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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.