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JunD proto-oncogene, AP-1 transcription factor subunit (JUND) is a member of the JUN family of transcription factors and a functional component of the Activator Protein-1 (AP-1) complex [1, 2]. Unlike other members of the family, JUND is often constitutively expressed and plays a complex role in regulating cell proliferation, apoptosis, and the response to oxidative stress [1, 3]. In many pathological states, such as certain cancers (e.g., prostate and breast cancer) and fibrotic diseases (e.g., liver and kidney fibrosis), JUND is upregulated, promoting disease progression by activating downstream pro-survival and pro-fibrotic genes [3, 4]. Targeting JUND at the mRNA level using antisense oligonucleotides or small interfering RNAs (siRNAs) represents a therapeutic strategy to reduce its protein expression and mitigate its pathological effects [5]. This approach is particularly relevant given the historical difficulty of targeting transcription factors with traditional small molecule inhibitors [5]. However, because JUND also has protective roles in normal physiology, such as maintaining redox balance, therapeutic intervention requires careful calibration to avoid systemic toxicity and off-target effects [1, 5].
Antisense-mediated mRNA degradation and RNA interference (RNAi) to reduce protein translation
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