ArticleGenes & cancer2013
The S100A4 Oncoprotein Promotes Prostate Tumorigenesis in a Transgenic Mouse Model: Regulating NFκB through the RAGE Receptor.
Article in Genes & cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- S100A4/FSP1: A Prognostic Marker and a Promising Target for Antitumor Therapy.International journal of molecular sciences · 2025Review
- Article
- Biological and clinical significance of the AGE-RAGE axis in the aggressiveness and prognosis of prostate cancer.Journal of food and drug analysis · 2023Article
- Review
- Molecular Insight into Prostate Cancer: Preventive Role of Selective Bioactive Molecules.Life (Basel, Switzerland) · 2023Review
- S100A4 Is Involved in Stimulatory Effects Elicited by the FGF2/FGFR1 Signaling Pathway in Triple-Negative Breast Cancer (TNBC) Cells.International journal of molecular sciences · 2021Article
- The role of S100A4 for bone metastasis in prostate cancer cells.BMC cancer · 2021Article
- Anti-S100A4 Antibody Therapy Is Efficient in Treating Aggressive Prostate Cancer and Reversing Immunosuppression: Serum and BiopsyMolecular cancer therapeutics · 2020Article
- Targeting AXL and RAGE to prevent geminin overexpression-induced triple-negative breast cancer metastasis.Scientific reports · 2019Article
- Characterization of Novel Murine and Human PDAC Cell Models: Identifying the Role of Intestine Specific Homeobox Gene ISX in Hypoxia and Disease Progression.Translational oncology · 2019Article
- Overexpression of S100A4 Predicts Migration, Invasion, and Poor Prognosis of Hypopharyngeal Squamous Cell Carcinoma.Molecular diagnosis & therapy · 2019Article
- Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Embigin Promotes Prostate Cancer Progression by S100A4-Dependent and-Independent Mechanisms.Cancers · 2018Article
- S100A4 Protects Myeloid-Derived Suppressor Cells from Intrinsic ApoptosisFrontiers in immunology · 2018Article
- S100A4 in cancer progression and metastasis: A systematic review.Oncotarget · 2017Review
- Extracellular S100A4 negatively regulates osteoblast function by activating the NF-κB pathway.BMB reports · 2017Article
- Deficiency in Calcium-Binding Protein S100A4 Impairs the Adjuvant Action of Cholera Toxin.Frontiers in immunology · 2017Article
- Melanoma Brain Metastasis: Mechanisms, Models, and Medicine.International journal of molecular sciences · 2016Review
- Article
- Orf Virus 002 Protein Targets Ovine Protein S100A4 and Inhibits NF-κB Signaling.Frontiers in microbiology · 2016Article
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Authors and funding
11 authors.
Funding
Abstract
S100A4, a calcium-binding protein, is known for its role in the metastatic spread of tumor cells, a late event of cancer disease. This is the first report showing that S100A4 is not merely a metastatic protein but also an oncoprotein that plays a critical role in the development of tumors. We earlier showed that S100A4 expression progressively increases in prostatic tissues with the advancement of prostate cancer (CaP) in TRAMP, an autochthonous mouse model. To study the functional significance of S100A4 in CaP, we generated a heterozygously deleted S100A4 (TRAMP/S100A4(+/-)) genotype by crossing TRAMP with S100A4(-/-) mice. TRAMP/S100A4(+/-) did not show a lethal phenotype, and transgenes were functional. As compared to age-matched TRAMP littermates, TRAMP/S100A4(+/-) mice exhibited 1) an increased tumor latency period (P < 0.001), 2) a 0% incidence of metastasis, and 3) reduced prostatic weights (P < 0.001). We generated S100A4-positive clones from S100A4-negative CaP cells and tested their potential. S100A4-positive tumors grew at a faster rate than S100A4-negative tumors in vitro and in a xenograft mouse model. The S100A4 protein exhibited growth factor-like properties in multimode (intracellular and extracellular) forms. We observed that 1) the growth-promoting effect of S100A4 is due to its activation of NFκB, 2) S100A4-deficient tumors exhibit reduced NFκB activity, 3) S100A4 regulates NFκB through the RAGE receptor, and 4) S100A4 and RAGE co-localize in prostatic tissues of mice. Keeping in view its growth-promoting role, we suggest that S100A4 qualifies as an excellent candidate to be exploited for therapeutic agents to treat CaP in humans.
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