ArticleNPJ precision oncology2021
Stabilization of p18 by deubiquitylase CYLD is pivotal for cell cycle progression and viral replication.
Article in NPJ precision oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed, 18 citations in OpenAlex.
- Toripalimab plus anlotinib in patients with recurrent or metastatic nasopharyngeal carcinoma: A multicenter, single-arm phase 2 trial (TORAL).Cell reports. Medicine · 2024Trial
- EBV-Driven ODC1 Upregulation Enhances Polyamine Anabolism to Promote Viral Replication and Cisplatin Resistance in Nasopharyngeal Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting MMA-induced USP36 methylmalonylation to suppress macrophage polarization and tumor progression in clear-cell renal cell carcinoma.Cell death and differentiation · 2026Article
- EBV (LMP1) enhances cisplatin resistance by enhancing degradation of interferon regulatory factor 3.Cell communication and signaling : CCS · 2026Article
- Functional mechanisms of circular RNA‑encoded peptides and future research strategies and directions in nasopharyngeal carcinoma (Review).International journal of oncology · 2025Review
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- Characterization of two melanoma cell lines resistant to BRAF/MEK inhibitors (vemurafenib and cobimetinib).Cell communication and signaling : CCS · 2024Article
- CIP/KIP and INK4 families as hostages of oncogenic signaling.Cell division · 2024Review
- CYLD induces high oxidative stress and DNA damage through class I HDACs to promote radiosensitivity in nasopharyngeal carcinoma.Cell death & disease · 2024Article
- A scATAC-seq atlas of stasis zone in rat skin burn injury wound process.Frontiers in cell and developmental biology · 2024Article
- USP38 inhibits colorectal cancer cell proliferation and migration via downregulating HMX3 ubiquitylation.Cell cycle (Georgetown, Tex.) · 2023Article
- Current methodologies in protein ubiquitination characterization: from ubiquitinated protein to ubiquitin chain architecture.Cell & bioscience · 2022Review
- CPT1A-mediated fatty acid oxidation promotes cell proliferation via nucleoside metabolism in nasopharyngeal carcinoma.Cell death & disease · 2022Article
- EBV Infection and Its Regulated Metabolic Reprogramming in Nasopharyngeal Tumorigenesis.Frontiers in cellular and infection microbiology · 2022Review
- NF-κB over-activation portends improved outcomes in HPV-associated head and neck cancer.Oncotarget · 2022Article
- Stabilization of p18 by deubiquitylase CYLD is pivotal for cell cycle progression and viral replication.NPJ precision oncology · 2021Article
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 4 countries.
Funding
Abstract
p18 is a key negative regulator of cell cycle progression and mediates cell cycle arrest at the G1/S phase. Ubiquitination is the prime mechanism in regulating p18 protein abundance. However, so far no post- translational regulator, especially DUBs, has been identified to regulate the protein stability of p18. In this paper, we identified CYLD as a deubiquitinase of p18, which binds to and removes the K48-linked polyubiquitylation chains conjugated onto p18, thus stabilizing the p18 protein. Loss of CYLD causes the degradation of p18 and induces the G1/S transition. Epstein-Barr virus (EBV), is the human oncovirus etiologically linked to nasopharyngeal carcinoma (NPC). Here we found that EBV drives a replication passive environment by deregulating the CYLD-p18 axis. Functionally, CYLD inhibits cell proliferation and tumorigenesis through p18 in vivo. Restoring CYLD prevents EBV induced viral replication and tumor growth. Collectively, our results identify CYLD directly stabilizes p18 to regulate the cellular G1/S transition. The reconstitution of CYLD-p18 axis could be a promising approach for EBV-positive cancer therapy.
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.