ArticleCell death & disease2021
FBXO16-mediated hnRNPL ubiquitination and degradation plays a tumor suppressor role in ovarian cancer.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 33 citations in OpenAlex.
- piR-26681 suppresses ovarian cancer progression by enhancing METTL3/METTL14-mediated mCellular & molecular biology letters · 2026Article
- Sex-stratified genetic regulators of cytokine production in the Dutch and Tanzanian populations.HGG advances · 2026Article
- Bidirectional regulation of the ubiquitin-RNA modification axis in cancer.Frontiers in oncology · 2026Review
- Harnessing Ribonucleoprotein Granule Biology for Cancer Therapy: The Central Role of Protein Modifications.Research (Washington, D.C.) · 2026Review
- Research advancements regarding the relationship between FBXO2 and malignant tumors (Review).Molecular medicine reports · 2025Review
- F-box proteins in cancer: from cancer cells to the tumor microenvironment.Cell communication and signaling : CCS · 2025Review
- Development of a 5K Liquid-Phase Genome-Wide Breeding Chip for Xinglong Buffalo.Animals : an open access journal from MDPI · 2025Article
- SENP3 protects hepatocyte from pyroptosis during acute liver injury through deSUMOylation of HNRNPL.iScience · 2025Article
- E3 ligase FBXW7 suppresses brown fat expansion and browning of white fat.EMBO reports · 2025Article
- RNA Sequencing Identifies Novel Signaling Pathways and Potential Drug Target Genes Induced by FOSL1 in Glioma Progression and Stemness.Biologics : targets & therapy · 2025Article
- Fbxo16 mediates degradation of NF-κB p65 subunit and inhibits inflammatory response in dendritic cells.Frontiers in immunology · 2025Article
- Protein ubiquitination in ovarian cancer immunotherapy: The progress and therapeutic strategy.Genes & diseases · 2024Review
- MIR937 amplification potentiates ovarian cancer progression by attenuating FBXO16 inhibition on ULK1-mediated autophagy.Cell death & disease · 2024Article
- Regulation of HNRNP family by post-translational modifications in cancer.Cell death discovery · 2024Review
- PTBP3 Mediates IL-18 Exon Skipping to Promote Immune Escape in Gallbladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- HMOX1: A pivotal regulator of prognosis and immune dynamics in ovarian cancer.BMC women's health · 2024Article
- Identification of hub genes and potential molecular mechanisms in MSS/MSI classifier primary colorectal cancer based on multiple datasets.Discover oncology · 2024Article
- FBXL18 is required for ovarian cancer cell proliferation and migration through activating AKT signaling.American journal of translational research · 2024Article
- Regulation of ovarian cancer by protein post-translational modifications.Frontiers in oncology · 2024Review
- Developments in Genetics: Better Management of Ovarian Cancer Patients.International journal of molecular sciences · 2023Review
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Heterogeneous nuclear ribonucleoprotein L (hnRNPL) is a type of RNA binding protein that highly expressed in a variety of tumors and plays a vital role in tumor progression. However, its post-translational regulation through ubiquitin-mediated proteolysis and the cellular mechanism responsible for its proteasomal degradation remains unclear. F-box proteins (FBPs) function as the substrate recognition subunits of SCF ubiquitin ligase complexes and directly bind to substrates. The aberrant expression or mutation of FBPs will lead to the accumulation of its substrate proteins that often involved in tumorigenesis. Here we discover FBXO16, an E3 ubiquitin ligase, to be a tumor suppressor in ovarian cancer, and patients with the relatively high expression level of FBXO16 have a better prognosis. Silencing or depleting FBXO16 significantly enhanced ovarian cancer cell proliferation, clonogenic survival, and cell invasion by activating multiple oncogenic pathways. This function requires the F-box domain of FBXO16, through which FBXO16 assembles a canonical SCF ubiquitin ligase complex that constitutively targets hnRNPL for degradation. Depletion of hnRNPL is sufficient to inactive multiple oncogenic signaling regulated by FBXO16 and prevent the malignant behavior of ovarian cancer cells caused by FBXO16 deficiency. FBXO16 interacted with the RRM3 domain of hnRNPL via its C-terminal region to trigger the proteasomal degradation of hnRNPL. Failure to degrade hnRNPL promoted ovarian cancer cell proliferation in vitro and tumor growth vivo, phenocopying the deficiency of FBXO16 in ovarian cancer.
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