ArticleOncotarget2014
βTrCP controls the lysosome-mediated degradation of CDK1, whose accumulation correlates with tumor malignancy.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 28 citations in OpenAlex.
- β-TrCP overexpression enhances cisplatin sensitivity by depleting BRCA1.Molecular oncology · 2026Article
- βTrCP facilitates MRN complex localization on chromatin to enhance DNA repair.Communications biology · 2025Article
- The antitumor peptide M1-20 induced the degradation of CDK1 through CUL4-DDB1-DCAF1-involved ubiquitination.Cancer gene therapy · 2025Article
- Baicalein sensitizes triple negative breast cancer MDA-MB-231 cells to doxorubicin via autophagy-mediated down-regulation of CDK1.Molecular and cellular biochemistry · 2023Article
- Targeting CDK1 in cancer: mechanisms and implications.NPJ precision oncology · 2023Review
- USP14 regulates cell cycle progression through deubiquitinating CDK1 in breast cancer.Acta biochimica et biophysica Sinica · 2022Article
- Inhibition of the CDK2 and Cyclin A complex leads to autophagic degradation of CDK2 in cancer cells.Nature communications · 2022Article
- Review
- Synthesis of new thienylpicolinamidine derivatives and possible mechanisms of antiproliferative activity.RSC advances · 2020Article
- Secreted breast tumor interstitial fluid microRNAs and their target genes are associated with triple-negative breast cancer, tumor grade, and immune infiltration.Breast cancer research : BCR · 2020Article
- Synthesis of new oxadiazol-phthalazinone derivatives with anti-proliferative activity; molecular docking, pro-apoptotic, and enzyme inhibition profile.RSC advances · 2020Article
- Proteomic Analysis of Protein Ubiquitination Events in Human Primary and Metastatic Colon Adenocarcinoma Tissues.Frontiers in oncology · 2020Article
- Cyclin F-dependent degradation of E2F7 is critical for DNA repair and G2-phase progression.The EMBO journal · 2019Article
- Identification of key modules and prognostic markers in adrenocortical carcinoma by weighted gene co-expression network analysis.Oncology letters · 2019Article
- Selective Autophagy Regulates Cell Cycle in Cancer Therapy.Theranostics · 2019Review
- Histone deacetylase inhibitors vorinostat and panobinostat induce G1 cell cycle arrest and apoptosis in multidrug resistant sarcoma cell lines.Oncotarget · 2017Article
- Both p62/SQSTM1-HDAC6-dependent autophagy and the aggresome pathway mediate CDK1 degradation in human breast cancer.Scientific reports · 2017Article
- The role of aberrant proteolysis in lymphomagenesis.Current opinion in hematology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, cell cycle progression is controlled by cyclin-dependent kinases, among which CDK1 plays important roles in the regulation of the G2/M transition, G1 progression and G1/S transition. CDK1 is highly regulated by its association to cyclins, phosphorylation and dephosphorylation, changes in subcellular localization, and by direct binding of CDK inhibitor proteins. CDK1 steady-state protein levels are held constant throughout the cell cycle by a coordinated regulation of protein synthesis and degradation. We show that CDK1 is ubiquitinated by the E3 ubiquitin ligase SCFβTrCP and degraded by the lysosome. Furthermore, we found that DNA damage not only triggers the stabilization of inhibitory phosphorylation sites on CDK1 and repression of CDK1 gene expression, but also regulates βTrCP-induced CDK1 degradation in a cell type-dependent manner. Specifically, treatment with the chemotherapeutic agent doxorubicin in certain cell lines provokes CDK1 degradation and induces apoptosis, whereas in others it inhibits destruction of the protein. These observations raise the possibility that different tumor types, depending on their pathogenic spectrum mutations, may display different sensitivity to βTrCP-induced CDK1 degradation after DNA damage. Finally, we found that CDK1 accumulation in patients' tumors shows a negative correlation with βTrCP and a positive correlation with the degree of tumor malignancy.
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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.