ArticleCommunications biology2020
FAM46C/TENT5C functions as a tumor suppressor through inhibition of Plk4 activity.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 32 citations in OpenAlex.
- TENT5C extends Odf1 poly(A) tail to sustain sperm morphogenesis and fertility.Nature communications · 2026Article
- Article
- TENT5C functions as a corepressor in the ligand-bound glucocorticoid receptor and estrogen receptor α complexes.The FEBS journal · 2025Article
- FAM46C Expression Sensitizes Multiple Myeloma Cells to PF-543-Induced Cytotoxicity.Biomolecules · 2025Article
- The emerging role of FAM46C as a biomarker and therapeutic target in gastric adenocarcinoma.Journal of gastrointestinal oncology · 2024Review
- Multi-dimensional characterization of apoptosis in the tumor microenvironment and therapeutic relevance in melanoma.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Article
- Dissecting the Puzzling Roles of FAM46C: A Multifaceted Pan-Cancer Tumour Suppressor with Increasing Clinical Relevance.Cancers · 2024Review
- FAM222A, Part of the BET-Regulated Basal Endothelial Transcriptome, Is a Novel Determinant of Endothelial Biology and Angiogenesis-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- FAM46C Is an Interferon-Stimulated Gene That Inhibits Lentiviral Particle Production by Modulating Autophagy.Microbiology spectrum · 2023Article
- Inhibition of FAM46/TENT5 activity by BCCIPα adopting a unique fold.Science advances · 2023Article
- Heme Metabolism-Related Gene TENT5C is a Prognostic Marker and Investigating Its Immunological Role in Colon Cancer.Pharmacogenomics and personalized medicine · 2023Article
- scDual-Seq ofFrontiers in immunology · 2023Article
- Centrosome Defects in Hematological Malignancies: Molecular Mechanisms and Therapeutic Insights.Blood science (Baltimore, Md.) · 2022Review
- Article
- FAM46C as a Potential Marker for Pan-Cancer Prognosis and Predicting Immunotherapeutic Efficacy.Frontiers in genetics · 2022Article
- Single-cell RNA sequencing reveals markers of disease progression in primary cutaneous T-cell lymphoma.Molecular cancer · 2021Article
- Structural and functional characterization of multiple myeloma associated cytoplasmic poly(A) polymerase FAM46C.Cancer communications (London, England) · 2021Article
- Centrosomes and cilia: always at the center of the action.Communications biology · 2020Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polo like kinase 4 (Plk4) is a tightly regulated serine threonine kinase that governs centriole duplication. Increased Plk4 expression, which is a feature of many common human cancers, causes centriole overduplication, mitotic irregularities, and chromosomal instability. Plk4 can also promote cancer invasion and metastasis through regulation of the actin cytoskeleton. Herein we demonstrate physical interaction of Plk4 with FAM46C/TENT5C, a conserved protein of unknown function until recently. FAM46C localizes to centrioles, inhibits Plk4 kinase activity, and suppresses Plk4-induced centriole duplication. Interference with Plk4 function by FAM46C was independent of the latter's nucleotidyl transferase activity. In addition, FAM46C restrained cancer cell invasion and suppressed MDA MB-435 cancer growth in a xenograft model, opposing the effect of Plk4. We demonstrate loss of FAM46C in patient-derived colorectal cancer tumor tissue that becomes more profound with advanced clinical stage. These results implicate FAM46C as a tumor suppressor that acts by inhibiting Plk4 activity.
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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.