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NFYB
NFYB Full Name
nuclear transcription factor Y, beta
NFYB Introduction
NFYB (nuclear transcription factor Y, beta) is one of the three core subunits of the NF-Y transcription factor complex, a highly conserved CCAAT-binding regulator widely present in eukaryotes. Together with NF-YA and NF-YC, NFYB forms a functional heterotrimer that binds promoter regions containing the CCAAT box, a common regulatory element in genes involved in cell cycle control, metabolism, and stress response. Structurally, NFYB contains a histone-fold domain (HFD), enabling protein–protein interactions not only within the NF-Y complex but also with other transcriptional regulators, thereby expanding its regulatory flexibility. Although NF-Y family expansion is particularly pronounced in plants, in humans NFYB remains a single-copy gene, underscoring its essential and non-redundant role in transcriptional regulation across fundamental biological processes.
Functionally, NFYB acts as a central transcriptional scaffold that stabilizes NF-YA binding to DNA and facilitates chromatin-associated gene activation or repression depending on interacting cofactors. Its regulatory influence extends to pathways governing proliferation, metabolic reprogramming, and mitochondrial activity. Recent single-cell transcriptomic analyses have highlighted NFYB as a key transcriptional regulator in high-proliferation tumor subpopulations, particularly in glioblastoma, where it is associated with enhanced oxidative phosphorylation and cell cycle progression. Mechanistically, NFYB can modulate tumor metabolic states and cell fate decisions through downstream effectors, including HDAC5-mediated transcriptional repression of metabolic enzymes such as SHMT2, linking transcriptional control directly to glycolytic balance and mitochondrial function.
Clinically, dysregulation of NFYB has been increasingly implicated in cancer progression, therapy response, and tumor recurrence, especially in glioblastoma multiforme (GBM), one of the most aggressive and treatment-resistant brain tumors. Evidence shows that NFYB knockdown suppresses GBM cell proliferation, invasion, and migration, while its overexpression can enhance chemosensitivity to temozolomide (TMZ) by reshaping metabolic pathways via the HDAC5/SHMT2 axis. However, NFYB-related transcriptional programs are also linked to tumor heterogeneity and poor prognosis in specific glioma subpopulations, indicating a context-dependent role in either tumor suppression or progression. These findings position NFYB as both a potential prognostic biomarker and a therapeutic entry point for targeting metabolic and transcriptional vulnerabilities in aggressive cancers.
Alternate Names for NFYB
NFYB; nuclear transcription factor Y, beta; nuclear transcription factor Y subunit beta; CBF A; HAP3; NF YB; Transcription factor NF-Y, B subunit; CAAT box DNA-binding protein subunit B; nuclear transcription factor Y subunit B; CCAAT-binding transcription factor subunit A; CBF-A; CBF-B; NF-YB;
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