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Far upstream element-binding protein 3 (FUBP3)
- Target
- FUBP3
- Molecular classification
- Transcription factor, Nucleic acid-binding protein, Other (regulator of gene expression)
01
Overview
Far upstream element-binding protein 3 (FUBP3) is a multifunctional nuclear protein that binds single-stranded DNA and RNA elements, modulating mRNA processing and gene transcription, especially at oncogenic loci such as the c-myc promoter[2][3][4]. FUBP3’s activity in the nucleus leads to regulation of cell proliferation, and it is implicated in cancer progression (including colorectal cancer, glioblastoma, and chronic myeloid leukemia) and in the replication/enhancement of certain viral infections[2][5]. In disease contexts, altered expression or copy number variations of FUBP3 can change cellular proliferation and modulate drug response, notably in leukemia[5]. While not a direct drug target, its role in disease-relevant pathways makes it a candidate for pathway-based therapeutic interventions and as a biomarker in oncology.
- Other names
- Far upstream element (FUSE) binding protein 3FBP3FUSE-binding protein 3FUBP3_HUMAN
02
Mechanism of action
Not applicable for direct drugs, but disease-modifying drugs act upstream/downstream of FUBP3—for example, ERK pathway inhibitors may interact with pathways regulated by FUBP3 in cancer.
03
Biological functions
Positive regulation of transcription by RNA polymerase IISingle-stranded DNA bindingRNA bindingmRNA maturation (regulation of transcript 3′ end processing)Cell proliferationViral RNA replication and translation regulationRegulation of the MAPK–ERK signaling pathway
04
Disease associations
Cancer (colorectal cancer, glioblastoma, chronic myeloid leukemia)Inflammation (ulcerative colitis)Viral infection (enterovirus 71, Japanese encephalitis virus, porcine epidemic diarrhea virus)Neuroprotection/neuronal developmentMuscle development (in pigs)
05
Safety considerations
Lack of direct safety concerns for therapies targeting FUBP3 since it is not (yet) a direct drug target. Therapeutic challenges are rather in modulating its associated pathways without off-target effects.
06
Interacting drugs
No direct therapeutic drugs are currently reported to target FUBP3 itself; however, its pathway interactions in diseases (e.g., via ERK/MAPK or PAK1 in CML) may render pathway inhibitors (such as tyrosine kinase inhibitors) relevant[5].
07
Biomarkers
FUBP3 expression/microdeletions as markers for poor response to tyrosine kinase inhibitors in chronic myeloid leukemia[5].Aberrant DNA methylation and expression in lung cancer, glioblastoma, and possibly in other cancers[2].
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