ArticleCancer research2010
Id2 promotes tumor cell migration and invasion through transcriptional repression of semaphorin 3F.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 92 citations in OpenAlex.
- Machine learning-predicted chromatin organization landscape across pediatric tumors.Scientific reports · 2026Article
- CRISP3, a Potential Tumor Suppressor, Inhibits the Progression of High-Grade Serous Ovarian Carcinoma by Modulating the PI3K/AKT Pathway.Biomedicines · 2026Article
- Pannexin 1 crosstalk with the Hippo pathway in malignant melanoma.The FEBS journal · 2025Article
- Pannexin 1 crosstalk with the Hippo pathway in malignant melanoma.bioRxiv : the preprint server for biology · 2024Article
- ID2-ETS2 axis regulates the transcriptional acquisition of pro-tumoral microglia phenotype in glioma.Cell death & disease · 2024Article
- The Roles of Antisense Long Noncoding RNAs in Tumorigenesis and Development through Cis-Regulation of Neighbouring Genes.Biomolecules · 2023Review
- Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.Biology · 2022Article
- GDF-11 promotes human trophoblast cell invasion by increasing ID2-mediated MMP2 expression.Cell communication and signaling : CCS · 2022Article
- Loss of E-cadherin leads to Id2-dependent inhibition of cell cycle progression in metastatic lobular breast cancer.Oncogene · 2022Article
- Semaphorin 3F induces colorectal cancer cell chemosensitivity by promoting P27 nuclear export.Frontiers in oncology · 2022Article
- Essential function and targets of BMP signaling during midbrain neural crest delamination.Developmental biology · 2021Article
- Androgen receptor signalling confers clonogenic and migratory advantages in urothelial cell carcinoma of the bladder.Molecular oncology · 2021Article
- SEMAPHORINS and their receptors: focus on the crosstalk between melanoma and hypoxia.Journal of experimental & clinical cancer research : CR · 2021Review
- MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis.International journal of molecular sciences · 2020Review
- Endothelial Semaphorin 3F Maintains Endothelial Barrier Function and Inhibits Monocyte Migration.International journal of molecular sciences · 2020Article
- Semaphorin 3F Promotes Transendothelial Migration of Leukocytes in the Inflammatory Response After Survived Cardiac Arrest.Inflammation · 2019Article
- ID2 and GJB2 promote early-stage breast cancer progression by regulating cancer stemness.Breast cancer research and treatment · 2019Article
- The RING domain in the anti-apoptotic protein XIAP stabilizes c-Myc protein and preserves anchorage-independent growth of bladder cancer cells.The Journal of biological chemistry · 2019Article
- Fates of CD8+ T cells in Tumor Microenvironment.Computational and structural biotechnology journal · 2019Review
- Analysis of chromatin accessibility uncovers TEAD1 as a regulator of migration in human glioblastoma.Nature communications · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Id proteins (Id1 to Id4) are helix-loop-helix transcription factors that promote metastasis. It was found that Semaphorin 3F (SEMA3F), a potent inhibitor of metastasis, was repressed by Id2. High metastatic human tumor cell lines had relatively high amounts of Id2 and low SEMA3F levels compared with their low metastatic counterparts. No correlation between metastatic potential and expression of the other Id family members was observed. Furthermore, ectopic expression of Id2 in low metastatic tumor cells downregulated SEMA3F and, as a consequence, enhanced their ability to migrate and invade, two requisite steps of metastasis in vivo. Id2 overexpression was driven by the c-myc oncoprotein. SEMA3F was a direct target gene of the E47/Id2 pathway. Two E-box sites, which bind E protein transcription factors including E47, were identified in the promoter region of the SEMA3F gene. E47 directly activated SEMA3F promoter activity and expression and promoted SEMA3F biological activities, including filamentous actin depolymerization, inactivation of RhoA, and inhibition of cell migration. Silencing of SEMA3F inhibited the E47-induced SEMA3F expression and biological activities, confirming that these E47-induced effects were SEMA3F dependent. E47 did not induce expression of the other members of the SEMA3 family. Id2, a dominant-negative inhibitor of E proteins, abrogated the E47-induced SEMA3F expression and biological activities. Thus, high metastatic tumor cells overexpress c-myc, leading to upregulation of Id2 expression; the aberrantly elevated amount of Id2 represses SEMA3F expression and, as a consequence, enhances the ability of tumor cells to migrate and invade.
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Registered trials
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.