ArticleJournal of hematology & oncology2018
The CCR4-NOT complex is a tumor suppressor in Drosophila melanogaster eye cancer models.
Article in Journal of hematology & oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- RNA kinetics influence the response to transcriptional perturbation in leukaemia cell lines.NAR cancer · 2024Article
- Specific tRNAs promote mRNA decay by recruiting the CCR4-NOT complex to translating ribosomes.Science (New York, N.Y.) · 2024Article
- Non-synonymous, synonymous, and non-coding nucleotide variants contribute to recurrently altered biological processes during retinoblastoma progression.Genes, chromosomes & cancer · 2023Article
- Processing body (P-body) and its mediators in cancer.Molecular and cellular biochemistry · 2022Review
- ThePlant physiology · 2020Article
- CCR4‑NOT transcription complex subunit 2 regulates TRAIL sensitivity in non‑small‑cell lung cancer cells via the STAT3 pathway.International journal of molecular medicine · 2020Article
- Dual Repressive Function by Cip1, a Budding Yeast Analog of p21, in Cell-Cycle START Regulation.Frontiers in microbiology · 2020Article
- Surveillance of Tumour Development: The Relationship Between Tumour-Associated RNAs and Ribonucleases.Frontiers in pharmacology · 2019Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe CNOT3 protein is a subunit of the CCR4-NOT complex, which is involved in mRNA degradation. We recently identified CNOT3 loss-of-function mutations in patients with T-cell acute lymphoblastic leukemia (T-ALL).
methodsHere, we use different Drosophila melanogaster eye cancer models to study the potential tumor suppressor function of Not3, the CNOT3 orthologue, and other members of the CCR4-NOT complex.
resultsOur data show that knockdown of Not3, the structural components Not1/Not2, and the deadenylases twin/Pop2 all result in increased tumor formation. In addition, overexpression of Not3 could reduce tumor formation. Not3 downregulation has a mild but broad effect on gene expression and leads to increased levels of genes involved in DNA replication and ribosome biogenesis. CycB upregulation also contributes to the Not3 tumor phenotype. Similar findings were obtained in human T-ALL cell lines, pointing out the conserved function of Not3.
conclusionsTogether, our data establish a critical role for Not3 and the entire CCR4-NOT complex as tumor suppressor.
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Registered trials
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