Basic transcription factor 3 (BTF3)

Basic transcription factor 3 (BTF3) is a multifunctional transcription factor required for the initiation of gene transcription by stabilizing RNA polymerase II complexes[1][2][7]. It possesses key DNA binding and activation domains, and alternative splicing produces multiple isoforms (e.g., BTF3a, BTF3b)[3][5]. Beyond its canonical function in transcription, BTF3 is involved in diverse cellular processes such as apoptosis modulation, cell cycle regulation, maintenance of stemness, autophagy regulation, and protein biogenesis through its action as part of the nascent polypeptide-associated complex[1][7]. Clinically, BTF3 is frequently overexpressed in a range of human cancers, where it promotes proliferation, impairs cell cycle control, and inhibits apoptosis[1][3]. Its levels serve as a biomarker of poor prognosis and are implicated in tumor sensitivity to chemotherapeutics. Thus, BTF3 is a promising molecular target for novel anti-cancer therapies, though direct drugs are still in experimental phases[1][3][6][7].

Other names

Transcription factor BTF3NACBOK/SW-cl.8NAC-betaBTF3aBTF3bNascent polypeptide-associated complex subunit betaRNA polymerase B transcription factor 3BETA-NACNascent-polypeptide-associated complex beta polypeptide

RNA interference constructs (siRNA or shRNA) lowering BTF3 expression suppress cancer cell growth and promote apoptosis. MicroRNAs, such as miR-802, inhibit BTF3 and suppress oncogenic functions. Potential small molecule interventions may disrupt the BTF3-transcriptional regulation complex, but these are in preclinical stages.