ArticleMolecular cancer research : MCR2017
Deubiquitinase OTUD6B Isoforms Are Important Regulators of Growth and Proliferation.
Article in Molecular cancer research : MCR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
- Targeting the OTU family: a core therapeutic strategy for reshaping the immunosuppressive microenvironment and reversing drug resistance in HCC by coordinating the autophagy-ferroptosis balance.Cell death discovery · 2026Review
- Proximity proteomics reveals OTUD6B regulation of stress granule dynamics through coalescence with VCP/p97.Cell death & disease · 2026Article
- Microbiome-Derived Metabolites Shape CD4bioRxiv : the preprint server for biology · 2026Article
- OTU deubiquitinases in disease: roles and targeting.Trends in molecular medicine · 2026Review
- Deubiquitomic and bioinformatic analyses in cisplatin-treated lung cancer cells.International journal of medical sciences · 2026Article
- Activation of Kv11.1 potassium channel suppresses non-small cell lung cancer growth by promoting c-Myc degradation.Communications biology · 2025Article
- OTU deubiquitinases in cancer pathogenesis and precision therapy.American journal of cancer research · 2025Review
- Deubiquitinating Enzyme OTUDs: Focus on Cancers and Antiviral Response.Oncology research · 2025Review
- OTUD6 deubiquitination of RPS7/eS7 on the free 40 S ribosome regulates global protein translation and stress.Nature communications · 2024Article
- The deubiquitinating protein OTUD6B promotes lung adenocarcinoma progression by stabilizing RIPK1.Biology direct · 2024Article
- Otud6b induces pulmonary arterial hypertension by mediating the Calpain-1/HIF-1α signaling pathway.Cellular and molecular life sciences : CMLS · 2024Article
- Deubiquitination of CDC6 by OTUD6A promotes tumour progression and chemoresistance.Molecular cancer · 2024Article
- An apicoplast-localized deubiquitinase contributes to the cell growth and apicoplast homeostasis of Toxoplasma gondii.Veterinary research · 2024Article
- All-Trans Retinoic Acid Promotes a Tumor Suppressive OTUD6B-β-TrCP-SNAIL Axis in Esophageal Squamous Cell Carcinoma and Enhances Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Gene transcriptional profiles in gonads of Bacillus taxa (Phasmida) with different cytological mechanisms of automictic parthenogenesis.Zoological letters · 2022Article
- YOD1 serves as a potential prognostic biomarker for pancreatic cancer.Cancer cell international · 2022Article
- Deubiquitylase OTUD6B stabilizes the mutated pVHL and suppresses cell migration in clear cell renal cell carcinoma.Cell death & disease · 2022Article
- Loss of OTUD6B Stimulates Angiogenesis and Promotes Diabetic Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Deubiquitinase OTUB2 exacerbates the progression of colorectal cancer by promoting PKM2 activity and glycolysis.Oncogene · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Deubiquitinases (DUB) are increasingly linked to the regulation of fundamental processes in normal and cancer cells, including DNA replication and repair, programmed cell death, and oncogenes and tumor suppressor signaling. Here, evidence is presented that the deubiquitinase OTUD6B regulates protein synthesis in non-small cell lung cancer (NSCLC) cells, operating downstream from mTORC1. OTUD6B associates with the protein synthesis initiation complex and modifies components of the 48S preinitiation complex. The two main OTUD6B splicing isoforms seem to regulate protein synthesis in opposing fashions: the long OTUD6B-1 isoform is inhibitory, while the short OTUD6B-2 isoform stimulates protein synthesis. These properties affect NSCLC cell proliferation, because OTUD6B-1 represses DNA synthesis while OTUD6B-2 promotes it. Mutational analysis and downstream mediators suggest that the two OTUD6B isoforms modify different cellular targets. OTUD6B-2 influences the expression of cyclin D1 by promoting its translation while regulating (directly or indirectly) c-Myc protein stability. This phenomenon appears to have clinical relevance as NSCLC cells and human tumor specimens have a reduced OTUD6B-1/OTUD6B-2 mRNA ratio compared with normal samples. The global OTUD6B expression level does not change significantly between nonneoplastic and malignant tissues, suggesting that modifications of splicing factors during the process of transformation are responsible for this isoform switch. IMPLICATIONS: Because protein synthesis inhibition is a viable treatment strategy for NSCLC, these data indicate that OTUD6B isoform 2, being specifically linked to NSCLC growth, represents an attractive, novel therapeutic target and potential biomarker for early diagnosis of malignant NSCLC. Mol Cancer Res; 15(2); 117-27. ©2016 AACR.
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