ArticleJournal of the National Cancer Institute2025
The nucleosome remodeling and deacetylase-SWItch/sucrose non-fermentable antagonism regulates the coordinated activation of epithelial-to-mesenchymal transition and inflammation in oral cancer.
Article in Journal of the National Cancer Institute, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Review
- C-terminal binding protein 2 interacts with JUNB to control macrophage inflammation.Life science alliance · 2025Article
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16 authors.
Funding
Abstract
backgroundPhenotypic plasticity and inflammation, 2 well-established hallmarks of cancer, play key roles in local invasion and distant metastasis by enabling the rapid adaptation of tumor cells to dynamic micro-environmental changes.
resultsHere, we show that in oral squamous carcinoma cell carcinoma (OSCC), the competition between the Nucleosome Remodeling and Deacetylase (NuRD) and SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complexes plays a pivotal role in regulating both epithelial-mesenchymal plasticity (EMP) and inflammation. By perturbing these complexes, we demonstrated their opposing downstream effects on the inflammatory pathways and EMP regulation. In particular, downregulation of the BRG1-specific SWI/SNF complex deregulates key inflammatory genes, such as TNF-α and IL6, in opposite ways when compared with the loss of CDK2AP1, a key member of the NuRD complex. We showed that CDK2AP1 genetic ablation triggers a pro-inflammatory secretome encompassing several chemokines and cytokines, thus promoting the recruitment of monocytes into the tumor microenvironment (TME). Furthermore, CDK2AP1 deletion stimulates their differentiation into M2-like macrophages, as validated on tumor microarrays from OSCC patient-derived tumor samples. Further analysis of the inverse correlation between CDK2AP1 expression and TME immune infiltration revealed specific downstream effects on the abundance and localization of CD68+ macrophages.
conclusionsOur study sheds light on the role of chromatin remodeling complexes in OSCC locoregional invasion and highlights the potential of CDK2AP1 and other members of NuRD and SWI/SNF chromatin remodeling complexes as prognostic markers and therapeutic targets.
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