ArticleCell & bioscience2021
DDB2 regulates DNA replication through PCNA-independent degradation of CDT2.
Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
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- Integrated analysis of ALK higher expression in human cancer and downregulation in LUAD using RNA molecular scissors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
- miR-34a negatively regulates cell cycle factor Cdt2/DTL in HPV infected cervical cancer cells.BMC cancer · 2022Article
- Gene co-expression network analysis revealed novel biomarkers for ovarian cancer.Frontiers in genetics · 2022Article
- Hypoxia-inducible CircPFKFB4 Promotes Breast Cancer Progression by Facilitating the CRL4International journal of biological sciences · 2022Article
- RIOK2 Inhibitor NSC139021 Exerts Anti-Tumor Effects on Glioblastoma via Inducing Skp2-Mediated Cell Cycle Arrest and Apoptosis.Biomedicines · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTargeting ubiquitin-dependent proteolysis is one of the strategies in cancer therapy. CRL
methodsSmall interfering RNAs were used to determine the function of target genes. Co-immunoprecipitation (Co-IP) was performed to detect the interaction between DDB2 and CDT2. Immunofluorescence assays and fluorescence activating cell sorting (FACS) were used to measure the change of DNA content. In vivo ubiquitination assay was carried out to clarify the ubiquitination of CDT2 mediated by DDB2. Cell synchronization was performed to arrest cells at G1/S and S phase. The mechanism involved in DDB2-mediated CDT2 degradation was investigated by constructing plasmids with mutant variants and measured by Western blot. Immunohistochemistry was performed to determine the relationship between DDB2 and CDT2. Paired two-side Student's t-test was used to measure the significance of the difference between control group and experimental group.
resultsKnockdown of DDB2 stabilized CDT2, while over-expression of DDB2 enhanced ubiquitination of CDT2, and subsequentially degradation of CDT2. Although both DDB2 and CDT2 contain PIP (PCNA-interacting protein) box, PIP box is dispensable for DDB2-mediated CDT2 degradation. Knockdown of PCNA had negligible effects on the stability of CDT2, but promoted accumulation of CDT1, p21 and SET8. Silencing of DDB2 arrested cell cycle in G1 phase, destabilized CDT1 and reduced the chromatin loading of MCMs, thereby blocked the formation of polyploidy induced by ablation of CDT2. In breast cancer and ovarian teratoma tissues, high level of DDB2 was along with lower level of CDT2.
conclusionsWe found that CRL4
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