ArticlePeerJ2025
Single-cell RNA-seq reveals breast cancer heterogeneity and identifies TCP1 as a therapeutic target in breast cancer.
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
5 authors.
Funding
Abstract
Breast cancer is composed of diverse cell populations, and this intratumoral heterogeneity profoundly affects clinical behavior. Here, we leveraged single cell RNA sequencing (scRNA-seq) of 68 breast cancer specimens to dissect tumor heterogeneity at high resolution. Unsupervised clustering identified all major cell types of the tumor microenvironment (TME)-including malignant epithelial cells, fibroblasts, T cells, macrophages, endothelial cells, and others-with striking variability in their proportions across molecular subtypes. For example, a BRCA1-mutant triple-negative breast cancer (TNBC) sample showed dense immune infiltration, whereas an estrogen receptor (ER)-positive tumor was mostly epithelial, consistent with known subtype differences in immunogenicity. We applied inference of copy number variations (inferCNV) to distinguish malignant epithelial cells, identifying ~90,000 tumor cells with significant copy-number aberrations enriched for cancer hallmark pathways. Re-clustering of these malignant cells revealed five discrete subpopulations. Notably, a KRT17-positive subcluster displayed the highest stemness score and a distinctive ETS-family transcription factor (ERG) regulon, suggesting a stem-like phenotype. Using The Cancer Genome Atlas (TCGA) cohort, we found that genes upregulated in this KRT17+ subpopulation, particularly NFKBIA, PDLIM4, and TCP1 stratified patient survival. An 8-gene risk signature derived from the KRT17 program segregated patients into high- and low-risk groups with markedly different outcomes. High-risk tumors were characterized by an immunosuppressive TME enriched in M2-like macrophages, whereas low-risk tumors more often harbored lymphocyte-predominant infiltrates. Focusing on TCP1, a chaperonin subunit upregulated in high-risk tumors, we demonstrate that TCP1 knockdown in breast cancer cell lines substantially impairs cell migration (~50% reduction in wound closure) and invasion (
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