ArticleInternational journal of molecular sciences2021
S100A4 Is Involved in Stimulatory Effects Elicited by the FGF2/FGFR1 Signaling Pathway in Triple-Negative Breast Cancer (TNBC) Cells.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Super enhancer lncRNA RP11-54O7.17 regulates the proliferation and metastasis of triple-negative breast cancer by targeting lysosomal degradation of S100A4.Cell death & disease · 2025Article
- S100A4/FSP1: A Prognostic Marker and a Promising Target for Antitumor Therapy.International journal of molecular sciences · 2025Review
- Article
- ANXA9 facilitates S100A4 and promotes breast cancer progression through modulating STAT3 pathway.Cell death & disease · 2024Article
- Therapies targeting triple-negative breast cancer: a perspective on anti-FGFR.Frontiers in oncology · 2024Review
- RAGE and its ligands in breast cancer progression and metastasis.Oncology reviews · 2024Review
- Review
- Article
- The tumor microenvironment and triple-negative breast cancer aggressiveness: shedding light on mechanisms and targeting.Expert opinion on therapeutic targets · 2022Article
- Triple-negative and triple-positive breast cancer cells reciprocally control their growth and migration via the S100A4 pathway.Cell adhesion & migration · 2022Article
- Article
- The RAGE/multiligand axis: a new actor in tumor biology.Bioscience reports · 2022Review
- TNBC: Potential Targeting of Multiple Receptors for a Therapeutic Breakthrough, Nanomedicine, and Immunotherapy.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) is an aggressive breast tumor subtype characterized by poor clinical outcome. In recent years, numerous advancements have been made to better understand the biological landscape of TNBC, though appropriate targets still remain to be determined. In the present study, we have determined that the expression levels of FGF2 and S100A4 are higher in TNBC with respect to non-TNBC patients when analyzing "The Invasive Breast Cancer Cohort of The Cancer Genome Atlas" (TCGA) dataset. In addition, we have found that the gene expression of FGF2 is positively correlated with S100A4 in TNBC samples. Performing quantitative PCR, Western blot, CRISPR/Cas9 genome editing, promoter studies, immunofluorescence analysis, subcellular fractionation studies, and ChIP assays, we have also demonstrated that FGF2 induces in TNBC cells the upregulation and secretion of S100A4 via FGFR1, along with the ERK1/2-AKT-c-Rel transduction signaling. Using conditioned medium from TNBC cells stimulated with FGF2, we have also ascertained that the paracrine activation of the S100A4/RAGE pathway triggers angiogenic effects in vascular endothelial cells (HUVECs) and promotes the migration of cancer-associated fibroblasts (CAFs). Collectively, our data provide novel insights into the action of the FGF2/FGFR1 axis through S100A4 toward stimulatory effects elicited in TNBC cells.
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Registered trials
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