<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>16</volume><submitter>Wang Z</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Cervical cancer (CC) is a major global health issue, ranking sixth in cancer-related mortality. The tumor microenvironment (TME) plays a crucial role in tumor growth. This study explored the cellular composition and immunological landscape of CC using various genomic data sources.&lt;h4>Methods&lt;/h4>Data from the Cancer Genome Atlas and Gene Expression Omnibus were analyzed, including single-cell RNA sequencing, spatial transcriptome analysis, and survival data. Gene set variation analysis (GSVA) identified pathways in CD8+ cells, macrophages, and epithelial cells. Immunohistochemistry assessed marker expression in CC and normal tissues. Tumor immune dysfunction and exclusion (TIDE) scores differentiated high- and low-macrophage groups. Cell-cell communication analyses highlighted interactions between macrophages and epithelial cells.&lt;h4>Results&lt;/h4>Macrophage markers correlated with overall survival (OS) and disease-free survival (DFS). Epithelial cell subgroups 1 and 4, along with CD8+ T cells, were associated with OS. TIDE scores varied between groups. Specific ligand-receptor interactions were found between macrophages and epithelial cell subgroup 1. Triptolide was effective in epithelial cell subgroup 1, while memantine was more effective in macrophages.&lt;h4>Conclusion&lt;/h4>Epithelial-macrophage interactions in the TME are crucial for CC progression and treatment, offering a potential immunotherapeutic strategy.</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>1537785</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12014682</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Epithelial and macrophage cell interaction in cervical cancer through single-cell RNA-sequencing and spatial analysis.</pubmed_title><pmcid>PMC12014682</pmcid><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Cheng L</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors><pubmed_authors>Cheng H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Epithelial and macrophage cell interaction in cervical cancer through single-cell RNA-sequencing and spatial analysis.</name><description>&lt;h4>Background&lt;/h4>Cervical cancer (CC) is a major global health issue, ranking sixth in cancer-related mortality. The tumor microenvironment (TME) plays a crucial role in tumor growth. This study explored the cellular composition and immunological landscape of CC using various genomic data sources.&lt;h4>Methods&lt;/h4>Data from the Cancer Genome Atlas and Gene Expression Omnibus were analyzed, including single-cell RNA sequencing, spatial transcriptome analysis, and survival data. Gene set variation analysis (GSVA) identified pathways in CD8+ cells, macrophages, and epithelial cells. Immunohistochemistry assessed marker expression in CC and normal tissues. Tumor immune dysfunction and exclusion (TIDE) scores differentiated high- and low-macrophage groups. Cell-cell communication analyses highlighted interactions between macrophages and epithelial cells.&lt;h4>Results&lt;/h4>Macrophage markers correlated with overall survival (OS) and disease-free survival (DFS). Epithelial cell subgroups 1 and 4, along with CD8+ T cells, were associated with OS. TIDE scores varied between groups. Specific ligand-receptor interactions were found between macrophages and epithelial cell subgroup 1. Triptolide was effective in epithelial cell subgroup 1, while memantine was more effective in macrophages.&lt;h4>Conclusion&lt;/h4>Epithelial-macrophage interactions in the TME are crucial for CC progression and treatment, offering a potential immunotherapeutic strategy.</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2025-07-02T03:05:06.407Z</modification><creation>2025-07-02T03:05:06.407Z</creation></dates><accession>S-EPMC12014682</accession><cross_references><pubmed>40270962</pubmed><doi>10.3389/fimmu.2025.1537785</doi></cross_references></HashMap>