ArticleOncoscience2014
Cancer driver candidate genes AVL9, DENND5A and NUPL1 contribute to MDCK cystogenesis.
Article in Oncoscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Molecular Imprints of Clinical Comorbidities in Hypothalamic Extracellular Vesicles at the Onset of Obesity.ACS omega · 2025Article
- Heterozygosity-Rich Regions in Canine Genome: Can They Serve as Indicators of Balancing Selection?Animals : an open access journal from MDPI · 2025Article
- Comprehensive Analysis of Prognostic Alternative Splicing Signatures in Tumor Immune Infiltration in Bladder Cancer.Recent patents on anti-cancer drug discovery · 2025Article
- Loss of symmetric cell division of apical neural progenitors drives DENND5A-related developmental and epileptic encephalopathy.Nature communications · 2024Article
- Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024Review
- Variant ranking pipeline for complex familial disorders.Scientific reports · 2024Article
- Loss of symmetric cell division of apical neural progenitors drivesmedRxiv : the preprint server for health sciences · 2024Article
- Circular RNA in Non-small Cell Lung Carcinoma: Identification of Targets and New Treatment Modalities.Cancer genomics & proteomics · 2023Review
- Shared hotspot mutations in oncogenes position dogs as an unparalleled comparative model for precision therapeutics.Scientific reports · 2023Article
- Induction of apically mistrafficked epiregulin disrupts epithelial polarity via aberrant EGFR signaling.Journal of cell science · 2021Article
- Canine tumor mutational burden is correlated with TP53 mutation across tumor types and breeds.Nature communications · 2021Article
- hsa_circ_0058357 acts as a ceRNA to promote non‑small cell lung cancer progression via the hsa‑miR‑24‑3p/AVL9 axis.Molecular medicine reports · 2021Article
- The lncRNA ALMS1-IT1 may promote malignant progression of lung adenocarcinoma via AVL9-mediated activation of the cyclin-dependent kinase pathway.FEBS open bio · 2021Article
- Biomarker potentials of miRNA-associated circRNAs in breast cancer (MCF-7) cells: an in vitro and in silico study.Molecular biology reports · 2021Article
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- Nucleoporin Nup58 localizes to centrosomes and mid-bodies during mitosis.Cell division · 2019Article
- Linc00662 Promotes Tumorigenesis and Progression by Regulating miR-497-5p/AVL9 Axis in Colorectal Cancer.Frontiers in genetics · 2019Article
- NUP58 facilitates metastasis and epithelial-mesenchymal transition of lung adenocarcinoma via the GSK-3β/Snail signaling pathway.American journal of translational research · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
AVL9, DENND5A and NUPL1 are among the cancer driver candidate genes previously identified via dog-human comparison, and may function in epithelial cell polarity as indicated by bioinformatics analysis. To better understand their cellular functions and roles in cancer, we knocked down each gene in MDCKII cells through shRNA and performed three-dimensional culture. Compared to the control, the knockdown clones developed significantly more abnormal cysts, e.g., cysts with the lumen harboring dead and/or live cells, or cysts having multiple lumens. Further analysis revealed that abnormalities initiated at the first cell division and persisted throughout the entire cystogenesis process. For NUPL1-knockdown cells, abnormal cytogenesis largely arose from faulty cell divisions, notably monopolar spindles or spindles with poorly separated poles. For AVL9- or DENND5A-knockdown cells, abnormalities originated from both aberrant intracellular trafficking and defective mitosis. Moreover, while all knockdown clones displayed an accelerated rate of both cell proliferation and death, only AVL9- and DENND5A-knockdowns, but not NUPL1-knockdown, promoted cell migration. These observations indicate that NUPL1 contributes to bipolar spindle formation, whereas AVL9 and DENND5A participate in both intracellular trafficking and cell cycle progression. Our study shed lights on these genes' normal cellular functions and on how their alteration contributes to carcinogenesis.
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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.