# Single-cell and multi-omics analyses identify CAMP-associated neutrophil remodeling during radiochemotherapy in cervical cancer

## TL;DR

This study shows that CAMP plays a key role in neutrophil changes during cervical cancer and its treatment, offering new insights into immune response and potential treatment strategies.

## Contribution

The study identifies CAMP as a novel regulator of neutrophil remodeling and tumor microenvironment dynamics during radiochemotherapy in cervical cancer.

## Key findings

- CAMP is highly expressed in cervical cancer tissues but decreases after radiochemotherapy.
- CAMP-high neutrophils show enhanced immune activation and communication with fibroblasts and epithelial cells.
- Radiochemotherapy suppresses CAMP-driven inflammatory and extracellular matrix signals in cervical cancer.

## Abstract

To investigate key genes and immune microenvironment dynamics in cervical cancer progression and radiochemotherapy (RCT), focusing on cathelicidin antimicrobial peptide (CAMP)-mediated neutrophil regulation.

Integrated transcriptomic data from TCGA, GTEx, and GEO were analyzed to identify differentially expressed genes associated with cervical cancer (CC) and RCT. Prognostic genes were selected via univariate and multivariate Cox regression. Single-cell RNA sequencing (scRNA-seq) characterized cellular composition, gene expression, and neutrophil subsets. CAMP-high and CAMP-low neutrophils were analyzed for differential expression, functional enrichment, pseudotime trajectories, and cell–cell communication.

Three prognostic genes (CAMP, CCDC116, and GLB1L3) were identified, with CAMP highly expressed in cervical cancer tissues but markedly downregulated after RCT. At the single-cell level, CAMP showed significant differential expression in tumor-associated and RCT-related neutrophils. Differential analysis and GO enrichment of neutrophils stratified by CAMP expression revealed enhanced innate immune activation, cytokine signaling, and granule secretion features following RCT. Pseudotime analysis demonstrated that CAMP expression gradually increased as neutrophils differentiated toward tumor-associated states, whereas it significantly decreased at terminal states after RCT. Cell–cell communication analysis further indicated that CAMP-high neutrophils exhibited strengthened signaling with fibroblasts and epithelial cells, particularly involving key ligands such as CXCL, COL1, and LAMC; RCT effectively suppressed tumor-specific inflammatory and extracellular matrix remodeling signals. In vitro experiments show that CAMP promotes malignant proliferation and activates inflammatory pathways in cervical cancer, whereas RCT suppresses these effects and modulates the COL1A1/COL1A2–CD44 and ANXA1–FPR1/FPR2 axes, reshaping tumor microenvironmental adhesion and immune activity.

CAMP is a key regulator of neutrophil differentiation and tumor immune microenvironment remodeling in cervical cancer and during RCT. Its modulation of cell–cell communication networks suggest potential as a biomarker for treatment response and a therapeutic target.