ArticleCommunications biology2023
NFYA promotes malignant behavior of triple-negative breast cancer in mice through the regulation of lipid metabolism.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 18 citations in OpenAlex.
- Activation of EZH2 Promoter Is Mediated by MAPK Signaling Regulated Transcription Factors in Anaplastic Thyroid Cancer.International journal of molecular sciences · 2026Article
- Single-nucleus and spatial transcriptomics analyses reveal interplay between evolutionary dynamics and energy metabolism in primary cardiac lymphoma.Cancer gene therapy · 2026Article
- Gene regulatory network transitions reveal the central transcription factors in lung adenocarcinoma progression.NPJ systems biology and applications · 2026Article
- Unveiling immune-related gene signatures in triple negative breast cancer through integrated transcriptomic analysis.BioMedicine · 2026Article
- Article
- Lipid Metabolism Reprogramming in Cancer: Insights into Tumor Cells and Immune Cells Within the Tumor Microenvironment.Biomedicines · 2025Review
- Lipid metabolism involved in progression and drug resistance of breast cancer.Genes & diseases · 2025Review
- Snord67 promotes breast cancer metastasis by guiding U6 modification and modulating the splicing landscape.Nature communications · 2025Article
- Article
- Metabolic Reprogramming and Adaption in Breast Cancer Progression and Metastasis.Advances in experimental medicine and biology · 2025Review
- NFYA-mediated promotion of castration-resistant prostate cancer progression through EGR4 regulation.Discover oncology · 2024Article
- Paracrine Signaling Mediated by the Cytosolic Tryparedoxin Peroxidase ofPathogens (Basel, Switzerland) · 2024Article
- Therapeutic protein PAK restrains the progression of triple negative breast cancer through degrading SREBP-1 mRNA.Breast cancer research : BCR · 2023Article
- Challenges and Opportunities in Developing Targeted Therapies for Triple Negative Breast Cancer.Biomolecules · 2023Review
- NFYAv1 is a Tumor-Promoting Transcript Associated with Poor Prognosis of Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2023Article
- NFYA promotes the anti-tumor effects of gluconeogenesis in hepatocellular carcinoma through the regulation of PCK1 expression.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two splicing variants exist in NFYA that exhibit high expression in many human tumour types. The balance in their expression correlates with prognosis in breast cancer, but functional differences remain unclear. Here, we demonstrate that NFYAv1, a long-form variant, upregulates the transcription of essential lipogenic enzymes ACACA and FASN to enhance the malignant behavior of triple-negative breast cancer (TNBC). Loss of the NFYAv1-lipogenesis axis strongly suppresses malignant behavior in vitro and in vivo, indicating that the NFYAv1-lipogenesis axis is essential for TNBC malignant behavior and that the axis might be a potential therapeutic target for TNBC. Furthermore, mice deficient in lipogenic enzymes, such as Acly, Acaca, and Fasn, exhibit embryonic lethality; however, Nfyav1-deficient mice exhibited no apparent developmental abnormalities. Our results indicate that the NFYAv1-lipogenesis axis has tumour-promoting effects and that NFYAv1 may be a safe therapeutic target for TNBC.
Indexed as
Identifiers
What OpenQuestion holds
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.