ArticleAnnals of surgical oncology2025
SPARC Induces COL1A1/COL3A1 Expressions Representing Aggressive Molecular Cancer-Associated Fibroblasts Signatures and CSF1-Mediated Cancer Invasion in Colorectal Cancer.
Article in Annals of surgical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Cancer-associated fibroblast-derived POSTN as a metabolic "switch" shapes lipid-stressed macrophage polarization in gastric cancer.Redox biology · 2026Article
- Endothelial Cell Heterogeneity in Carotid Plaque Calcification: An Exploratory Single-Cell Transcriptomic Study with Proteomic Support.International journal of general medicine · 2026Article
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Authors and funding
32 authors.
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Abstract
backgroundSecreted protein, acidic and rich in cysteine (SPARC) may play an important role in tumor microenvironment (TME) contribution to metastasis, however molecular mechanism of SPARC contribution to TME remains elusive. EXPERIMENTAL
designIn this study, SPARC molecular status was explored for its clinical and functional relevance to metastasis in the context of its stromal overexpression, which may represent colorectal cancer (CRC) progression.
resultsSPARC expression was highly specific to cancer stroma of CRC tumors (GSE35608) and exhibited prognostic relevance. SPARC knockdown (KD) in cancer-associated fibroblasts (CAFs) resulted in diminished metastatic phenotypes, accompanied by robust suppression of COL1A1/COL3A1 expressions and multiple secretome genes. Among the secretome genes, CSF1 was closely associated with stromal SPARC expression, and it was demonstrated that the CSF1/CSF1R axis was required for SPARC-induced cancer invasion. Comprehensive selection by stromal specificity and its SPARC association identified CAF-associated genes (CAFGs), including classical CAFs markers and COL family genes, which were uniquely enriched as higher priority for prognosis. These findings suggest that SPARC-mediated induction of COL family genes and secretome in the TME may be primarily featured against the host rather than be protective.
conclusionsOur present findings may aid in simplifying molecular understanding of aggressive TME and enrich bona-fide therapeutic targets for cancer metastasis.
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