ArticleMolecular and cellular biology2000
TEL, a putative tumor suppressor, modulates cell growth and cell morphology of ras-transformed cells while repressing the transcription of stromelysin-1.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 106 citations in OpenAlex.
- ETV6 mutations in early immature human T cell leukemias.The Journal of experimental medicine · 2011Trial
- The novel ETV6::RARA fusion gene, identified in acute promyelocytic leukemia, is sensitive to invitro all-tans retinoic acid and arsenic trioxide administrations.Annals of hematology · 2026Article
- Article
- Article
- Inherited Thrombocytopenia Related Genes: GPS2 Mediates the Interplay Between ANKRD26 and ETV6.Cells · 2024Article
- The Diverse Roles of ETV6 Alterations in B-Lymphoblastic Leukemia and Other Hematopoietic Cancers.Advances in experimental medicine and biology · 2024Review
- The ETS transcription factor ETV6 constrains the transcriptional activity of EWS-FLI to promote Ewing sarcoma.Nature cell biology · 2023Article
- ETV6-related thrombocytopenia: dominant negative effect of mutations as common pathogenic mechanism.Haematologica · 2022Article
- Article
- Establishment of a transgenic mouse to model ETV7 expressing human tumors.Transgenic research · 2019Article
- Identification of novel recurrent ETV6-IgH fusions in primary central nervous system lymphoma.Neuro-oncology · 2018Article
- Pathogenesis of ETV6/RUNX1-positive childhood acute lymphoblastic leukemia and mechanisms underlying its relapse.Oncotarget · 2017Review
- ETV6 in hematopoiesis and leukemia predisposition.Seminars in hematology · 2017Review
- CLIC5: a novel ETV6 target gene in childhood acute lymphoblastic leukemia.Haematologica · 2016Article
- Germline mutations in ETV6 are associated with thrombocytopenia, red cell macrocytosis and predisposition to lymphoblastic leukemia.Nature genetics · 2015Article
- Germline ETV6 mutations in familial thrombocytopenia and hematologic malignancy.Nature genetics · 2015Article
- Pachymic acid modified carbon nanoparticles reduced angiogenesis via inhibition of MMP-3.International journal of clinical and experimental pathology · 2015Article
- Haploinsufficiency of ETV6 and CDKN1B in patients with acute myeloid leukemia and complex karyotype.BMC genomics · 2014Article
- Autoinhibition of ETV6 (TEL) DNA binding: appended helices sterically block the ETS domain.Journal of molecular biology · 2012Article
- The leukemia-associated fusion protein MN1-TEL blocks TEL-specific recognition sequences.PloS one · 2012Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
TEL is a member of the ETS family of transcription factors that interacts with the mSin3 and SMRT corepressors to regulate transcription. TEL is biallelically disrupted in acute leukemia, and loss of heterozygosity at the TEL locus has been observed in various cancers. Here we show that expression of TEL in Ras-transformed NIH 3T3 cells inhibits cell growth in soft agar and in normal cultures. Unexpectedly, cells expressing both Ras and TEL grew as aggregates. To begin to explain the morphology of Ras-plus TEL-expressing cells, we demonstrated that the endogenous matrix metalloproteinase stromelysin-1 was repressed by TEL. TEL bound sequences in the stromelysin-1 promoter and repressed the promoter in transient-expression assays, suggesting that it is a direct target for TEL-mediated regulation. Mutants of TEL that removed a binding site for the mSin3A corepressor but retained the ETS domain failed to repress stromelysin-1. When BB-94, a matrix metalloproteinase inhibitor, was added to the culture medium of Ras-expressing cells, it caused a cell aggregation phenotype similar to that caused by TEL expression. In addition, TEL inhibited the invasiveness of Ras-transformed cells in vitro and in vivo. Our results suggest that TEL acts as a tumor suppressor, in part, by transcriptional repression of stromelysin-1.
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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.