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Interleukin enhancer-binding factor 2 (ILF2/NF45) is a 45 kDa transcription factor and RNA-binding protein predominantly located in the nucleus and highly expressed in testis, brain, and kidney[1]. ILF2 forms a heterodimer with ILF3 (NF90/NF110), which is critical for T cell activation by promoting interleukin 2 expression through binding specific enhancer elements. It regulates multiple aspects of RNA and DNA metabolism, including transcriptional control, mRNA processing, stabilization, alternative splicing, miRNA biogenesis, and DNA damage repair[1][2][5]. Overexpression or amplification of ILF2 is associated with malignancy (especially multiple myeloma and pancreatic carcinoma), genomic instability, and resistance to DNA-damaging therapies. ILF2 functions as an autoantigen in some autoimmune diseases and facilitates viral replication for hepatitis B. It is considered a potential therapeutic target and biomarker in cancer and immune dysregulation, though safety and specificity challenges exist for therapeutic development[1][2][3][5].
Inhibition of ILF2 by upregulating microRNA-7 (curcumin). Therapeutic strategies aimed at disrupting its RNA-binding/transcriptional activity, leading to reduced oncogenicity and cell growth.
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