ArticleJournal of biomedical science2014
Up-regulation of S100A16 expression promotes epithelial-mesenchymal transition via Notch1 pathway in breast cancer.
Article in Journal of biomedical science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 52 citations in OpenAlex.
- Integrated bioinformatics and immunohistochemical analysis reveal that S100A16 is correlated with mutational burden, immune evasion, andInternational journal of clinical and experimental pathology · 2026Article
- Nucleolar proteomics identifies S100A16 as a key nucleolar protein driving breast cancer metastasis.Cell death & disease · 2025Article
- Mechanisms of microRNA Regulation of the Epithelial-Mesenchymal Transition (EMT) in Lung Cancer.Life (Basel, Switzerland) · 2024Review
- Notch signaling pathway in cancer: from mechanistic insights to targeted therapies.Signal transduction and targeted therapy · 2024Review
- Potential drug targets for tumors identified through Mendelian randomization analysis.Scientific reports · 2024Article
- Expression and gene regulatory network of S100A16 protein in cervical cancer cells based on data mining.BMC cancer · 2023Article
- Expression of S100A16 Is Associated with Biological Aggressiveness and Poor Prognosis in Patients with Bladder Cancer Who Underwent Radical Cystectomy.International journal of molecular sciences · 2023Article
- S100s and HMGB1 Crosstalk in Pancreatic Cancer Tumors.Biomolecules · 2023Article
- An Update on S100A16 in Human Cancer.Biomolecules · 2023Review
- Article
- RAGE Inhibitors for Targeted Therapy of Cancer: A Comprehensive Review.International journal of molecular sciences · 2022Review
- TRPC5OS induces tumorigenesis by increasing ENO1-mediated glucose uptake in breast cancer.Translational oncology · 2022Article
- Science CommuniCaCells · 2022Review
- Exosomes and Brain Metastases: A Review on Their Role and Potential Applications.International journal of molecular sciences · 2021Review
- ADAMTS19 Suppresses Cell Migration and Invasion by Targeting S100A16 via the NF-κB Pathway in Human Gastric Cancer.Biomolecules · 2021Article
- S100A16 suppresses the proliferation, migration and invasion of colorectal cancer cells in part via the JNK/p38 MAPK pathway.Molecular medicine reports · 2021Article
- Bivalent Genes Targeting of Glioma Heterogeneity and Plasticity.International journal of molecular sciences · 2021Review
- Integrated analysis identifies S100A16 as a potential prognostic marker for pancreatic cancer.American journal of translational research · 2021Article
- Calcium Binding Protein S100A16 Expedites Proliferation, Invasion and Epithelial-Mesenchymal Transition Process in Gastric Cancer.Frontiers in cell and developmental biology · 2021Article
- Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOur previous studies demonstrated that S100A16 promotes adipogenesis and is involved in weight gain attenuation induced by dietary calcium. Till now, the function of S100A16 in the breast cancer remains to be elucidated.
resultsIn this study, we observed that S100A16 was expressed in higher levels in human breast cancer tissues compared with paired adjacent non-cancerous tissues. Further examination showed that overexpression of S100A16 in MCF-7 cells could increase cell proliferation and colony formation. One major mechanistic change was that S100A16 was able to up-regulate the transcription factors Notch1, ZEB1, and ZEB2, which had the capacities to directly repress the expression of epithelial markers E-cadherin and β-catenin but increase mesenchymal markers N-cadherin and vimentin, a characterized phenotype of epithelial-mensenchymal transition (EMT). In addition to display with morphologic change, migration and invasion were increased in S100A16 over-expressed MCF-7 cells. Importantly, knockdown of Notch1 by specific siRNA could reverse the EMT induced by S100A16 overexpression, which confirmed that Notch1 played a critical role in the process of EMT induced by S100A16.
conclusionsAll together, our data indicated that S100A16 had a potential function to regulate some embryonic transcription factors to promote EMT in breast cancer cells which may be an important target site for the therapy of breast cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.