Authors
Qi Cao, Yuange Duan
Published in
The Journal of biological chemistry. Pages 113569. Sep 17, 2026. Epub Sep 17, 2026.
Abstract
Tumor-associated neutrophils (TANs) play dual roles in cancer progression, yet the molecular basis of their reprogramming by tumor cells remains poorly understood. Here, we performed a time-resolved transcriptomic and RNA editome analysis of neutrophils co-cultured with three hepatocellular carcinoma (HCC) cell lines using 293T cells as control. We observed consistent transcriptional remodeling across treatments, with progressive upregulation of pro-tumor genes and downregulation of anti-tumor genes, which were associated with functions of neutrophil chemotaxis, NETosis, metabolic reprogramming, and N1-to-N2 polarization. Concurrently, global A-to-I RNA editing, ADAR expression, together with ADAR1-MDA5-immunity and ADAR2-recoding axes were markedly reduced in HCC-induced neutrophils, compatible with the tumor-driven reprogramming hypothesis. Differential editing analysis revealed three key downregulated recoding sites with distinct evolutionary histories, MED21 (p.Gln145Arg), HSPA1L (p.Asn153Asp), and ZNF397 (p.Tyr481Cys), which may alter transcriptional and stress-regulatory functions of downstream targets. Together, these results indicate a possible link between transcriptional remodeling, RNA editing, and functional polarization of HCC-induced neutrophils. Since our analyses are in silico, the proposed mechanistic links should be interpreted as hypotheses for future validation. Our findings provide an exploratory framework for investigating ADAR-regulated RNA editing in tumor-immune communication.
PMID:
42754162
Bibliographic data and abstract were imported from PubMed on 18 Sep 2026.
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