ArticleNeoplasia (New York, N.Y.)2012
CAND1 promotes PLK4-mediated centriole overduplication and is frequently disrupted in prostate cancer.
Article in Neoplasia (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- GSDME acts as an epigenetic modifier to promote melanoma development via centriole biogenesis regulator PLK4.Cell death and differentiation · 2026Article
- Review
- ASCC3 promotes the immunosuppression and progression of non-small cell lung cancer by impairing the type I interferon response via CAND1-mediated ubiquitination inhibition of STAT3.Journal for immunotherapy of cancer · 2023Article
- Bioinformatics Analysis of the Prognostic Significance of CAND1 in ERα-Positive Breast Cancer.Diagnostics (Basel, Switzerland) · 2022Article
- Centrosome Defects in Hematological Malignancies: Molecular Mechanisms and Therapeutic Insights.Blood science (Baltimore, Md.) · 2022Review
- PLK4 is upregulated in prostate cancer and its inhibition reduces centrosome amplification and causes senescence.The Prostate · 2022Article
- Hypoxia Drives Centrosome Amplification in Cancer Cells via HIF1α-dependent Induction of Polo-Like Kinase 4.Molecular cancer research : MCR · 2022Article
- Article
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- Down-regulation of Polo-like kinase 4 (PLK4) induces G1 arrest via activation of the p38/p53/p21 signaling pathway in bladder cancer.FEBS open bio · 2021Article
- Review
- Post-Translational Modifications That Drive Prostate Cancer Progression.Biomolecules · 2021Review
- Polo-Like Kinase 4's Critical Role in Cancer Development and Strategies for Plk4-Targeted Therapy.Frontiers in oncology · 2021Review
- Rapid Ex-Vivo Ciliogenesis and Dose-Dependent Effect of Notch Inhibition on Ciliogenesis of Respiratory Epithelia.Biomolecules · 2020Article
- The Impact of Cand1 in Prostate Cancer.Cancers · 2020Article
- Gartanin is a novel NEDDylation inhibitor for induction of Skp2 degradation, FBXW2 expression, and autophagy.Molecular carcinogenesis · 2020Article
- Polo‑like kinase 4 promotes tumorigenesis and induces resistance to radiotherapy in glioblastoma.Oncology reports · 2019Article
- High PLK4 expression promotes tumor progression and induces epithelial‑mesenchymal transition by regulating the Wnt/β‑catenin signaling pathway in colorectal cancer.International journal of oncology · 2019Article
- MiR-126 negatively regulates PLK-4 to impact the development of hepatocellular carcinoma via ATR/CHEK1 pathway.Cell death & disease · 2018Article
- ACGH detects distinct genomic alterations of primary intrahepatic cholangiocarcinomas and matched lymph node metastases and identifies a poor prognosis subclass.Scientific reports · 2018Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Centrosomes play a crucial role in the maintenance of genome stability by orchestrating bipolar mitotic spindle formation. The centrosome normally duplicates precisely once before mitosis in a process that is extensively regulated by protein degradation including SKP1-Cullin 1 (CUL1)-F-box (SCF) E3 ubiquitin ligase activity. The core SCF component CUL1 has recently been found to be required to suppress the formation of supernumerary centrosomes and centrioles, the core-forming units of centrosomes. Here, we identify the CUL1-interacting protein cullin-associated and neddylation-dissociated 1 (CAND1) as a novel centrosomal protein with a role in centriole duplication control. CAND1 was found to synergize with Polo-like kinase 4 (PLK4), a master regulator of centriole biogenesis, in the induction of centriole overduplication. We provide evidence that CAND1 functions in this process by increasing PLK4 protein stability. Furthermore, mutants of CUL1 that lack the ability to interact with CAND1 and are unable to assemble functional E3 ubiquitin ligase complexes were impaired in their ability to restrain aberrant daughter centriole synthesis. To corroborate a role of CAND1 in human carcinogenesis, we analyzed a series of prostate adenocarcinomas and found altered expression of CAND1 on the mRNA or protein level in 52.9% and 40.8%, respectively, of the tumor samples analyzed. These results highlight the role of altered SCF components in cancer in general and encourage further studies to explore the SCF-CAND1 axis for the development of novel predictive biomarkers and therapeutic approaches in prostate cancer.
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