ArticleMolecular cancer research : MCR2014
ID1 promotes breast cancer metastasis by S100A9 regulation.
Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 58 citations in OpenAlex.
- Serum S100A8/S100A9 is associated with increased risk of brain metastasis in patients with inflammatory breast cancer.medRxiv : the preprint server for health sciences · 2026Article
- Telomere Maintenance and Oncogenesis.International journal of molecular sciences · 2025Review
- Ferulic acid inhibits ox-LDL-induced ferroptosis and apoptosis in RAW 264.7 cells via the HIF-1 signaling pathway.Frontiers in pharmacology · 2025Article
- Loss of tumor-derived SMAD4 enhances primary tumor growth but not metastasis following BMP4 signalling.Cell communication and signaling : CCS · 2024Article
- Article
- CircRNA circ_0006156 inhibits the metastasis of prostate cancer by blocking the ubiquitination of S100A9.Cancer gene therapy · 2022Article
- Article
- The Effect of Hypoxic and Normoxic Culturing Conditions in Different Breast Cancer 3D Model Systems.Frontiers in bioengineering and biotechnology · 2021Article
- Genomic integrity of human induced pluripotent stem cells across nine studies in the NHLBI NextGen program.Stem cell research · 2020Article
- High expression of ID1 in monocytes is strongly associated with phenotypic and functional MDSC markers in advanced melanoma.Cancer immunology, immunotherapy : CII · 2020Article
- Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy.International journal of medical sciences · 2020Review
- Lung-Seeking Metastases.Cancers · 2019Review
- The application of ApcJournal of cancer research and clinical oncology · 2019Review
- Prognostic values of the inhibitor of DNA‑binding family members in breast cancer.Oncology reports · 2018Article
- Identification of tumor-autonomous and indirect effects of vitamin D action that inhibit breast cancer growth and tumor progression.The Journal of steroid biochemistry and molecular biology · 2018Review
- Co-Incidence of Epstein-Barr Virus and High-Risk Human Papillomaviruses in Cervical Cancer of Syrian Women.Frontiers in oncology · 2018Article
- Inhibitor of DNA binding proteins: implications in human cancer progression and metastasis.American journal of translational research · 2018Review
- ID1 contributes to cell growth invasion and migration in salivary adenoid cystic carcinoma.Molecular medicine reports · 2017Article
- Article
- For robust big data analyses: a collection of 150 important pro-metastatic genes.Chinese journal of cancer · 2017Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledMetastasis is a major factor responsible for mortality in patients with breast cancer. Inhibitor of DNA binding 1 (Id1) has been shown to play an important role in cell differentiation, tumor angiogenesis, cell invasion, and metastasis. Despite the data establishing Id1 as a critical factor for lung metastasis in breast cancer, the pathways and molecular mechanisms of Id1 functions in metastasis remain to be defined. Here, we show that Id1 interacts with TFAP2A to suppress S100A9 expression. We show that expression of Id1 and S100A9 is inversely correlated in both breast cancer cell lines and clinical samples. We also show that the migratory and invasive phenotypes in vitro and metastasis in vivo induced by Id1 expression are rescued by reestablishment of S100A9 expression. S100A9 also suppresses the expression of known metastasis-promoting factor RhoC activated by Id1 expression. Our results suggest that Id1 promotes breast cancer metastasis by the suppression of S100A9 expression. IMPLICATIONS: Novel pathways by Id1 regulation in metastasis.
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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.