ArticleNature communications2017
The non-canonical poly(A) polymerase FAM46C acts as an onco-suppressor in multiple myeloma.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 112 citations in OpenAlex.
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- The TENT5A-ATXN2 axis modulates germline and somatic cell survival during heat stress.Cell death & disease · 2026Article
- The C-terminal region of TENT5 proteins drives ER-associated mRNA polyadenylation via FNDC3 interaction.Cell reports · 2026Article
- TENT-5 polyadenylates and regulates male-specific transcripts in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2026Article
- Plasma Proteomics Reveals Persistent and Surgery-Responsive Molecular Signatures in Osteoarthritis Patients.International journal of molecular sciences · 2026Article
- DIS3 mutations enhance AID-driven translocations during B-cell activation, promoting transformation to multiple myeloma.Nature communications · 2026Article
- Review
- TENT5C functions as a corepressor in the ligand-bound glucocorticoid receptor and estrogen receptor α complexes.The FEBS journal · 2025Article
- Article
- FAM46C Expression Sensitizes Multiple Myeloma Cells to PF-543-Induced Cytotoxicity.Biomolecules · 2025Article
- DIS3L, cytoplasmic exosome catalytic subunit, is essential for development but not cell viability in mice.RNA (New York, N.Y.) · 2025Article
- TENT5A mediates the cancer-inhibiting effects of EGR1 by suppressing the protein stability of RPL35 in hepatocellular carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Genetic architecture of oral glucose-stimulated insulin release provides biological insights into type 2 diabetes aetiology.Nature metabolism · 2024Article
- The emerging role of FAM46C as a biomarker and therapeutic target in gastric adenocarcinoma.Journal of gastrointestinal oncology · 2024Review
- TENT5-mediated polyadenylation of mRNAs encoding secreted proteins is essential for gametogenesis in mice.Nature communications · 2024Article
- RNA-binding proteins and exoribonucleases modulating miRNA in cancer: the enemy within.Experimental & molecular medicine · 2024Review
- Dissecting the Puzzling Roles of FAM46C: A Multifaceted Pan-Cancer Tumour Suppressor with Increasing Clinical Relevance.Cancers · 2024Review
- RNA processing mechanisms contribute to genome organization and stability in B cells.Oncogene · 2024Review
- Single-Cell Transcriptome Analysis Reveals Development-Specific Networks at Distinct Synchronized Antral Follicle Sizes in Sheep Oocytes.International journal of molecular sciences · 2024Article
- The Genetic and Molecular Drivers of Multiple Myeloma: Current Insights, Clinical Implications, and the Path Forward.Pharmacogenomics and personalized medicine · 2024Review
6 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
FAM46C is one of the most frequently mutated genes in multiple myeloma. Here, using a combination of in vitro and in vivo approaches, we demonstrate that FAM46C encodes an active non-canonical poly(A) polymerase which enhances mRNA stability and gene expression. Reintroduction of active FAM46C into multiple myeloma cell lines, but not its catalytically-inactive mutant, leads to broad polyadenylation and stabilization of mRNAs strongly enriched with those encoding endoplasmic reticulum-targeted proteins and induces cell death. Moreover, silencing of FAM46C in multiple myeloma cells expressing WT protein enhance cell proliferation. Finally, using a FAM46C-FLAG knock-in mouse strain, we show that the FAM46C protein is strongly induced during activation of primary splenocytes and that B lymphocytes isolated from newly generated FAM46C KO mice proliferate faster than those isolated from their WT littermates. Concluding, our data clearly indicate that FAM46C works as an onco-suppressor, with the specificity for B-lymphocyte lineage from which multiple myeloma originates. FAM46C is one of the most frequently mutated genes in multiple myeloma (MM), but its molecular function remains unknown. Here the authors show that FAM46C is a poly(A) polymerase and that loss of function of FAM46C drives multiple myeloma through the destabilisation of ER response transcripts.
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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.