ArticleNature communications2025
Constitutive expression of the transcriptional co-activator IκBζ promotes melanoma growth and immunotherapy resistance.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The impactful role of the HDACs in the regulation of gene expression and as targets for disease therapy.Science advances · 2026Review
- It's Not Rewarding for Mitochondria: Dopamine-Induced Mitochondrial Dysfunction Activates cGAS-STING to Drive IL-6 Secretion in Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Spatial Treg niches and the therapeutic reprogramming of tumour tolerance in cancer.Frontiers in cell and developmental biology · 2026Review
- The resilient subset: cancer stem cells at the core of immunotherapy resistance.Immunotherapy advances · 2026Review
- HDAC2 restrains IGF2BP1-associated m6A dysregulation in cervical cancer immunotherapy resistance.PloS one · 2026Article
- Wnt3a-expressing cancer stem cells impair CD8Oncoimmunology · 2025Article
- CC/CXC chemokine risk signature at single-cell resolution: a machine learning model for precision stratification in cervical cancer.Translational cancer research · 2025Article
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Authors and funding
20 authors.
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Abstract
IκBζ, a rather unknown co-regulator of NF-κB, can either activate or repress a subset of NF-κB target genes. While its role as an inducibly expressed, transcriptional regulator of cytokines and chemokines in immune cells is established, IκBζ's function in solid cancer remains unclear. Here we show that IκBζ protein is constitutively expressed in a subfraction of melanoma cell lines, and around 30% of all melanoma cases, independently of its mRNA levels or known mutations. Deleting IκBζ in melanoma abrogates the activity and chromatin association of STAT3 and NF-κB, thereby reducing the expression of the pro-proliferative cytokines IL-1β and IL-6, thus impairing melanoma cell growth. Additionally, IκBζ suppresses Cxcl9, Cxcl10, and Ccl5 expression via HDAC3 and EZH2, which impairs the recruitment of NK and CD8
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