ArticleFrontiers in medicine2026
STC1 promotes colorectal cancer invasion and migration by regulating M2 macrophage polarization via TGF-β1/Smad signaling pathway.
Article in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.
- Artemotil Attenuates Fibrosis-Associated Chondrocyte Remodelling in Osteoarthritis in Association With STC1-Related TGF-β/SMAD2/3 Signalling.Journal of cellular and molecular medicine · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Colorectal cancer (CRC) mortality is largely attributable to invasion, migration, and an immunosuppressive tumor microenvironment. We examined the clinical relevance and mechanistic function of stanniocalcin-1 (STC1) in CRC, with emphasis on macrophage polarization. Methods: STC1 expression patterns, prognostic value, and associated pathways were analyzed in TCGA and GEO CRC datasets, followed by KEGG enrichment. STC1 was silenced in HCT116 and SW620 cells using siRNA. Wound-healing and Transwell migration/invasion assays, immunofluorescence, qRT-PCR, ELISA and Western blotting were performed to evaluate metastatic phenotypes, epithelial-mesenchymal transition (EMT), and TGF-β1/Smad signaling. Correlations between STC1 and immune infiltration were assessed in TCGA. Conditioned-medium and co-culture experiments, together with flow cytometry analysis of M2-associated surface markers were used to determine the impact of STC1 on macrophage polarization and the reciprocal effects of polarized macrophages on CRC cell behavior. Results: STC1 was significantly upregulated in CRC, and high STC1 expression was associated with worse overall and disease-free survival. STC1 knockdown markedly reduced CRC cell migration and invasion and attenuated EMT, as evidenced by increased E-cadherin and decreased N-cadherin/vimentin. Bioinformatic and experimental analyses indicated that STC1 promotes CRC progression via activation of the TGF-β1/Smad pathway. STC1 levels correlated positively with macrophage infiltration in CRC tissues. Conclusion: STC1 facilitates CRC invasion and migration by activating TGF-β1/Smad signaling and driving M2 macrophage polarization, suggesting its utility as a prognostic biomarker and therapeutic target.
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