ArticleNature communications2024
Aggresome formation promotes ASK1/JNK signaling activation and stemness maintenance in ovarian cancer.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- HOXC9 accelerates esophageal squamous cell carcinoma progression via OTUD1-FABP5-mediated lipid metabolic reprogramming.Cell death & disease · 2026Article
- Raw defines a TIR-fold cADPR hydrolase cooperating with dSarm in development and axon degeneration.Cell communication and signaling : CCS · 2026Article
- USP16 regulates mitochondrial function by deubiquitinating TOM40, a core component of the translocase in the mitochondrial outer membrane.Cell death & disease · 2026Article
- Targeting cancer stem cells predicts response and reverses chemoresistance in ascites-derived ovarian cancer organoids.BMC medicine · 2026Article
- The role of OTUD1-mediated deubiquitination in disease pathogenesis: from molecular mechanisms to clinical translation.Frontiers in immunology · 2026Review
- A positive feedback loop of OTUD1 and c-Jun driven by leptin expedites stemness maintenance in ovarian cancer.Oncogene · 2025Article
- Lamins regulate cancer cell plasticity and chemosensitivity.Frontiers in oncology · 2025Article
- Stemness-driven clusters in ovarian cancer: immune characteristics and prognostic implications.Frontiers in oncology · 2025Article
- Dissecting the dual role of OTU family proteins in tumor progression and immune escape.Frontiers in immunology · 2025Review
- Review
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Aggresomes are the product of misfolded protein aggregation, and the presence of aggresomes has been correlated with poor prognosis in cancer patients. However, the exact role of aggresomes in tumorigenesis and cancer progression remains largely unknown. Herein, the multiomics screening reveal that OTUD1 protein plays an important role in retaining ovarian cancer stem cell (OCSC) properties. Mechanistically, the elevated OTUD1 protein levels lead to the formation of OTUD1-based cytoplasmic aggresomes, which is mediated by a short peptide located in the intrinsically disordered OTUD1 N-terminal region. Furthermore, OTUD1-based aggresomes recruit ASK1 via protein-protein interactions, which in turn stabilize ASK1 in a deubiquitinase-independent manner and activate the downstream JNK signaling pathway for OCSC maintenance. Notably, the disruption of OTUD1-based aggresomes or treatment with ASK1/JNK inhibitors, including ibrutinib, an FDA-approved drug that was recently identified as an MKK7 inhibitor, effectively reduced OCSC stemness (OSCS) of OTUD1
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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 Socratic graph.