ArticleCell death discovery2022
Deubiquitylase OTUD1 confers Erlotinib sensitivity in non-small cell lung cancer through inhibition of nuclear translocation of YAP1.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
17 citing papers in PubMed, 17 citations in OpenAlex.
- The role of OTUD1-mediated deubiquitination in disease pathogenesis: from molecular mechanisms to clinical translation.Frontiers in immunology · 2026Review
- Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.American journal of cancer research · 2026Review
- OTU deubiquitinases as immune-circuit editors: from human immunopathology to therapeutic prioritization.Frontiers in immunology · 2026Review
- Role of the SOX family in non‑small cell lung cancer: Molecular mechanisms and therapeutic implications (Review).Oncology reports · 2026Review
- The deubiquitinase OTUD1 orchestrates cisplatin chemosensitivity of non-small cell lung cancer through destabilizing RAD23B/XPC.Oncogene · 2025Article
- Research progress of DUB enzyme in breast cancer.Clinical and experimental medicine · 2025Review
- METTL3‑mediated m6A methylation and its impact on OTUD1 expression in chronic obstructive pulmonary disease.Molecular medicine reports · 2025Article
- Posttranslational modifications of YAP/TAZ: molecular mechanisms and therapeutic opportunities.Cellular & molecular biology letters · 2025Review
- AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025Review
- Dissecting the dual role of OTU family proteins in tumor progression and immune escape.Frontiers in immunology · 2025Review
- Deubiquitinating Enzyme OTUDs: Focus on Cancers and Antiviral Response.Oncology research · 2025Review
- OTU deubiquitinases in cancer pathogenesis and precision therapy.American journal of cancer research · 2025Review
- Review
- The Role of Mechanotransduction in Contact Inhibition of Locomotion and Proliferation.International journal of molecular sciences · 2024Review
- VE-822 upregulates the deubiquitinase OTUD1 to stabilize FHL1 to inhibit the progression of lung adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Pleiotropic Roles of a KEAP1-Associated Deubiquitinase, OTUD1.Antioxidants (Basel, Switzerland) · 2023Review
- The roles of protein ubiquitination in tumorigenesis and targeted drug discovery in lung cancer.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence exists suggesting tumor-inhibiting properties of deubiquitylase OTUD1 in various malignancies. We herein investigated the anti-tumor effect and clarified the downstream mechanisms of OTUD1 in the chemoresistance of non-small cell lung cancer (NSCLC) cells. Expression of OTUD1 was examined in NSCLC (PC-9 cells) and erlotinib-resistant NSCLC (PC-9/ER) cell lines. OTUD1 was bioinformatically predicted to be weakly expressed in NSCLC tissue samples and verified in PC-9/ER cells. PC-9/ER cells were subsequently subjected to ectopic expression of OTUD1 alone or combined with SOX9 to dissect out the effect of OTUD1 on the proliferation, chemoresistance and apoptosis in vitro and in vivo. OTUD1 upregulation sensitized NSCLC cells to erlotinib both in vitro and in vivo. In the presence of OTUD1 overexpression, nuclear translocation of YAP1 was inhibited and its expression was inactivated. This effect of OTUD1 was associated with the decreased ubiquitination level of YAP1. SOX9/SPP1 inactivation was the consequence of inhibited nuclear translocation of YAP1. Overexpression of SOX9 reversed the inhibitory effect of OTUD1 on the resistance of NSCLC cells to erlotinib. In conclusion, our study reveals that OTUD1 potentially acts as a tumor suppressor and suppresses erlotinib resistance of NSCLC through the YAP1/SOX9/SPP1 axis, suggesting that OTUD1 may serve as a target for reducing chemoresistance for NSCLC.
Identifiers
What OpenQuestion holds
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.