Evidence map›Paper›PMID 42524145›Full record

ArticleJournal of Cancer2026

Single-cell Transcriptomics Uncovers the Tumor Microenvironment and Collagen-CD44 Axis in HIV Positive Cervical Squamous Cell Carcinoma.

Yuxi Ma, Lijun Zhang, Liangfei Niu, Bo Yan, Min Liu

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Article in Journal of Cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Yuxi MaDepartment of Obstetrics and Gynecology, Shanghai Public Health Clinical Center, Fudan University, Shanghai 201508, China.
Lijun ZhangShanghai Public Health Clinical Center, Fudan University, Shanghai 201508, China.
Liangfei NiuCenter for Tuberculosis Research, Shanghai Public Health Clinical Center, Fudan University, Shanghai 201508, China.
Bo YanCenter for Tuberculosis Research, Shanghai Public Health Clinical Center, Fudan University, Shanghai 201508, China.
Min LiuDepartment of Obstetrics and Gynecology, Shanghai Public Health Clinical Center, Fudan University, Shanghai 201508, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Human immunodeficiency virus (HIV) infection markedly increases the incidence and worsens clinical outcomes of cervical squamous cell carcinoma (CSCC). The single-cell landscape of the tumor microenvironment (TME) in HIV positive CSCC (HIV-CSCC) remains poorly defined, and its cellular and molecular differences from HIV negative CSCC are largely unclear. Methods: We performed single-cell RNA sequencing (scRNA-seq) on tumor tissues from three HIV-CSCC patients without preoperative chemoradiotherapy. Public scRNA-seq data of three HIV negative CSCC cases were integrated as controls. We systematically analyzed cellular composition, transcriptional profiles, metabolic characteristics and intercellular communication networks across groups. Results: Epithelial cells in HIV-CSCC exhibited aggravated malignant phenotypes and metabolic disorders. The C5 epithelial subcluster was strongly associated with poor patient survival. Tumor-infiltrating T cells displayed impaired cytotoxic function. Macrophages predominantly polarized into immunosuppressive M2-like phenotypes with attenuated phagocytosis and antigen presentation. Cancer-associated fibroblasts (CAFs) acted as the core regulatory hub in HIV-CSCC TME and mediated cell crosstalk mainly via the collagen-CD44 signaling axis. Upregulated CD44 was an independent prognostic factor for unfavorable survival in HIV positive patients. Conclusions: HIV-CSCC is characterized by a highly immunosuppressive TME and extensive stromal remodeling driven by activated CAFs. The collagen-CD44 pathway plays a key role in tumor progression. Our findings reveal the molecular mechanism of HIV-CSCC and identify CD44 as a promising therapeutic target for this disease.

Indexed as

CD44cervical squamous cell carcinomaHIVsingle-cell RNA sequencingtumor microenvironment

Identifiers

PMID42524145
PMCPMC13410425

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