ArticleInternational journal of oncology2019
S100A9 promotes the proliferation and migration of cervical cancer cells by inducing epithelial‑mesenchymal transition and activating the Wnt/β‑catenin pathway.
Article in International journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 29 citations in OpenAlex.
- Secreted protein combination GAPDH/S100A8/S100A9 from human expanded potential stem cells counteracts mesenchymal stromal cell senescence.Stem cell research & therapy · 2026Article
- Mesenchymal stem cell-induced metabolic reprogramming of EGFR-wild-type tumor cells drives therapeutic resistance in EGFR-mutant non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Differential Expression of S100A Genes in hDPSCs Following Stimulation with Two Hydraulic Calcium Silicate Cements: A Laboratory Investigation.Journal of functional biomaterials · 2026Article
- Charting the immune terrain: a novel risk model for thyroid cancer prognosis.Frontiers in genetics · 2026Article
- S100A9 as a promising therapeutic target for diabetic foot ulcers.Chinese medical journal · 2025Article
- Advances in S100 protein family for gynecological malignancies.Discover oncology · 2025Review
- The presence of glutathione S-transferase in recombinant S100A9 alters its effect on human sperm function.Journal of biomedical research · 2025Article
- Integrating multimodal cancer data using deep latent variable path modelling.Nature machine intelligence · 2025Article
- Article
- Advances in the study of S100A9 in cardiovascular diseases.Cell proliferation · 2024Review
- The role of S100A8 and S100A9 in external auditory canal cholesteatoma.Frontiers in immunology · 2024Article
- Multiomic analysis of cervical squamous cell carcinoma identifies cellular ecosystems with biological and clinical relevance.Nature genetics · 2023Article
- Joint analysis of the metabolomics and transcriptomics uncovers the dysregulated network and develops the diagnostic model of high-risk neuroblastoma.Scientific reports · 2023Article
- Nuclear proinflammatory cytokine S100A9 enhances expression of human papillomavirus oncogenes via transcription factor TEAD1.Journal of virology · 2023Article
- Integrated MicroRNA and Secretome Analysis of Human Endometrial Organoids Reveal the miR-3194-5p/Aquaporin/S100A9 Module in Regulating Trophoblast Functions.Molecular & cellular proteomics : MCP · 2023Article
- S100A9 promotes glycolytic activity in HER2-positive breast cancer to induce immunosuppression in the tumour microenvironment.Heliyon · 2023Article
- Downregulation of S100A9 Reverses Cisplatin-Resistance and Inhibits Proliferation and Migration in Hypopharyngeal Carcinoma.Journal of oncology · 2022Article
- Identification S100A9 as a potential biomarker in neuroblastoma.Molecular biology reports · 2021Article
- Review
- Contribution of RAGE axis activation to the association between metabolic syndrome and cancer.Molecular and cellular biochemistry · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100 calcium‑binding protein A9 (S100A9), a member of the S100 protein family, is often upregulated in various cancers, including cervical cancer. Elevated S100A9 expression is thought to serve an important role in tumorigenesis; however, the exact role of S100A9 in the modulation of cervical cancer and the underlying molecular mechanism remain unknown. In the present study, we aimed to investigate the effects of S100A9 on the proliferation and migration of cervical cancer cells, as well as the molecular mechanisms underlying these effects. Our results demonstrated that endogenous expression of S100A9 in SiHa and CaSki cell lines was significantly higher than in the HeLa cell line. As expected, overexpression of S100A9 enhanced the proliferation and migration of cervical cancer cells. In addition, S100A9 overexpression induced epithelial‑mesenchymal transition (EMT) as determined by reduced expression levels of the epithelial marker E‑cadherin, whereas the expression levels of the mesenchymal marker vimentin were upregulated. Furthermore, it was reported that the effects of S100A9 in the modulation of cervical cancer cells were mediated through the Wnt/β‑catenin signaling pathway as β‑catenin knockdown significantly suppressed the ability of S100A9 to enhance the proliferation and migration of cervical cancer cells. Collectively, these findings suggest that S100A9 promoted the proliferation and migration of cervical cancer cell lines. Furthermore, the underlying molecular mechanisms may be partially attributed to the induction of EMT and activation of the Wnt/β‑catenin signaling pathway.
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