ArticleCarcinogenesis2014
Id2, Id3 and Id4 overcome a Smad7-mediated block in tumorigenesis, generating TGF-β-independent melanoma.
Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- Catestatin peptide impedes melanoma progression and drug resistance by reprogramming oncogenic signaling pathways.Oncogenesis · 2026Article
- Catestatin peptide impedes melanoma progression and drug resistance by reprogramming oncogenic signaling pathways.Research square · 2026Article
- A prevalent disease-associated SNP in the humanNAR molecular medicine · 2026Article
- Catestatin suppresses melanoma progression and drug resistance through multitargeted modulation of signaling pathways.bioRxiv : the preprint server for biology · 2025Article
- FGFR1 variants contributed to families with tooth agenesis.Human genomics · 2023Article
- Employing CRISPR-Cas9 to Generate CD133 Synthetic Lethal Melanoma Stem Cells.International journal of molecular sciences · 2022Article
- Human melanocyte development and melanoma dedifferentiation at single-cell resolution.Nature cell biology · 2021Article
- Genome-wide CRISPR screens reveal cyclin C as synthetic survival target of BRCA2.Nucleic acids research · 2021Article
- Globally learning gene regulatory networks based on hidden atomic regulators from transcriptomic big data.BMC genomics · 2020Article
- Wogonin reverses the drug resistance of chronic myelogenous leukemia cells to imatinib through CXCL12-CXCR4/7 axis in bone marrow microenvironment.Annals of translational medicine · 2020Article
- Comparative gene expression analysis in melanocytes driven by tumor cell-derived exosomes.Experimental cell research · 2020Article
- Overexpressed VEPH1 inhibits epithelial-mesenchymal transition, invasion, and migration of human cutaneous melanoma cells through inactivating the TGF-β signaling pathway.Cell cycle (Georgetown, Tex.) · 2019Article
- CRISPR-Cas9 Knockdown and Induced Expression of CD133 Reveal Essential Roles in Melanoma Invasion and Metastasis.Cancers · 2019Article
- Single-Cell Mobility Analysis of Metastatic Breast Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2018Article
- CD71+VISTA+ erythroid cells promote the development and function of regulatory T cells through TGF-β.PLoS biology · 2018Article
- Hyaluronic acid-CD44 interactions promote BMP4/7-dependent Id1/3 expression in melanoma cells.Scientific reports · 2018Article
- New susceptibility loci for cutaneous melanoma risk and progression revealed using a porcine model.Oncotarget · 2018Article
- Alpha-1-antitrypsin functions as a protective factor in preeclampsia through activating Smad2 and inhibitor of DNA binding 4.Oncotarget · 2017Article
- Id2 Collaborates with Id3 To Suppress Invariant NKT and Innate-like Tumors.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- TGFΒ-induced transcription in cancer.Seminars in cancer biology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The role for the inhibitors of differentiation (Ids) proteins in melanomagenesis has been poorly explored. In other cell types, Ids have been shown to contribute to cell proliferation, migration and angiogenesis and, along with a number of other genes, are direct downstream targets of the transforming growth factor (TGF)-β pathway. Expression of Smad7, which suppress TGF-β signaling, or synthetic TGF-β inhibitors, was shown to potently suppress melanomagenesis. We found that endogenous Id2, Id3 and Id4 expression was elevated in 1205Lu versus 1205Lu cells constitutively expressing Smad7, indicating Ids may play a role in melanomagenesis. Therefore, the effects of Tet-inducible expression of Id2, Id3 or Id4 along with Smad7 in TGF-β-dependent 1205Lu human melanoma cells were explored in vitro and in vivo. 1205Lu cells formed subcutaneous tumors in athymic mice, whereas cells expressing Smad7 failed to form tumors. However, 1205Lu cells expressing Smad7 along with doxycycline-induced Id2, Id3 or Id4 were able to overcome the potent tumorigenic block mediated by S7, to varying degrees. Conversely, Id small interfering RNA knockdown suppressed anchorage-independent growth of melanoma. Histology of tumors from 1205Lu cells expressing Smad7 + Id4 revealed an average of 31% necrosis, compared with 5.2% in tumors from 1205Lu with vector only. Downstream, Ids suppressed cyclin-dependent kinase inhibitors, and re-upregulated invasion and metastasis-related genes matrix metalloproteinase 2 (MMP2), MMP9, CXCR4 and osteopontin, shown previously to be downregulated in response to Smad7. This study shows that Id2, Id3 and Id4 are each able to overcome TGF-β dependence, and establish a role for Ids as key mediators of TGF-β melanomagenesis.
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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.