ArticleAmerican journal of translational research2019
Degradation of CCNB1 mediated by APC11 through UBA52 ubiquitination promotes cell cycle progression and proliferation of non-small cell lung cancer cells.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
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- Competitive Binding of UBA52 and HOPX Modulates β-catenin Stability in Colorectal Cancer in the Context of High-Iron Intake.International journal of biological sciences · 2026Article
- The prognostic and neuroendocrine implications of SLC25A29-mediated biomass signature in prostate cancer.GeroScience · 2025Article
- Comprehensive analysis and experimental validation of disulfidptosis-associated prognostic signature and immune microenvironment characterization of gastric cancer.Cancer immunology, immunotherapy : CII · 2025Article
- INTS7 modulates cell proliferation and apoptosis via promoting cell cycle progression in lung adenocarcinoma.Briefings in functional genomics · 2025Article
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- MicroRNA-542-3p targets Pten to inhibit the myoblasts proliferation but suppresses myogenic differentiation independent of targeted Pten.BMC genomics · 2024Article
- Inhibition of UBA52 induces autophagy via EMC6 to suppress hepatocellular carcinoma tumorigenesis and progression.Journal of cellular and molecular medicine · 2024Article
- Surrogate Biomarker Prediction from Whole-Slide Images for Evaluating Overall Survival in Lung Adenocarcinoma.Diagnostics (Basel, Switzerland) · 2024Article
- Spatial transcriptomics analysis identifies therapeutic targets in diffuse high-grade gliomas.Frontiers in molecular neuroscience · 2024Article
- Identification of Key Prognostic Alternative Splicing Events of Costimulatory Molecule-Related Genes in Colon Cancer.Combinatorial chemistry & high throughput screening · 2024Article
- Methoxylated Cinnamic Esters with Antiproliferative and Antimetastatic Effects on Human Lung Adenocarcinoma Cells.Life (Basel, Switzerland) · 2023Article
- Cyclin B1 expression as an independent prognostic factor for lung adenocarcinoma and its potential pathways.Oncology letters · 2022Article
- Age-related Huntington's disease progression modeled in directly reprogrammed patient-derived striatal neurons highlights impaired autophagy.Nature neuroscience · 2022Article
- Zinc supplementation prevents mitotic accumulation in human keratinocyte cell lines upon environmentally relevant arsenic exposure.Toxicology and applied pharmacology · 2022Article
- MiR-139-5p Targeting CCNB1 Modulates Proliferation, Migration, Invasion and Cell Cycle in Lung Adenocarcinoma.Molecular biotechnology · 2022Article
- Analysis of the key prognostic genes and potential traditional Chinese medicine therapeutic targets in glioblastoma based on bioinformatics and network pharmacology methods.Translational cancer research · 2022Article
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- IdentifyingQuantitative imaging in medicine and surgery · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMechanism by which CCNB1 regulates the cell cycle progression and its prognostic function in non-squamous non-small cell lung cancer (NSCLC) are necessary to be further elucidated.
methodsData retrieved from gene expression omnibus (GEO) and cancer genome atlas (TCGA) combined with clinical data were used. Survival analysis was conducted in public datasets. Proteomics and co-immunoprecipation assays were designed to unravel proteins with interaction with CCNB1. Short hairpin RNA and small interfering RNA as well as overexpressing genes of interest were used.
resultsCCNB1 was not implicated in apoptosis, migration and invasion of NSCLC cells. After either knockdown or overexpression of CCNB1, the occurrence of cell cycle arrest in G2/M phase, fewer cloning formation and diminished dimension of xenograft tumors were observed. CCNB1 expression level was clinically associated with several clinicopathological parameters including gender, smoking, T stage and N stage. Survival analysis showed that the higher level of CCNB1, the more dismal outcome in overall survival as well as in disease-free survival. Mechanistically, we confirmed that the role of CCNB1 on cell cycle and cloning formation was dependent on UBA52, which was able to promote degradation of CCNB1; nevertheless, this consequence relied on APC11. Knockdown of APC11 led to cell cycle arrest in G2/M and less cloning formation even in the presence of overexpressed UBA52. Following upregulation of APC11, the protein of CCNB1 degraded with resultant cell cycle progression and more cloning formation.
conclusionDegradation of CCNB1 by APC11 via UBA52 ubiquitylation was critical in cell cycle progression and proliferation of NSCLC cell lines.
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Identifiers
31814919PMC6895529W3000438218What OpenQuestion holds
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.