ArticleBMC cancer2025
Deubiquitinase USP18 mediates cell migration, apoptosis and ferroptosis in lung adenocarcinoma by depending on POU4F1/PRKAA2 axis.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The mechanism of deubiquitinase USP14 modifying HSP90AA1 to activate NRF2 signaling in lung cancer cell resistance to ferroptosis.Molecular biology reports · 2026Article
- Deubiquitinases at the crossroads of ferroptosis and cancer therapy: mechanisms and therapeutic potential.Molecular biology reports · 2026Review
- Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.American journal of cancer research · 2026Review
- Prognostic value of neuro-related genes in colorectal cancer and their potential implications for immunotherapy.Journal of Cancer · 2026Article
- Review
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2 authors.
Funding
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Abstract
backgroundLung adenocarcinoma (LUAD) is a common type of lung cancer and its pathogenic mechanism is complicated. A profound research for the molecular mechanism in LUAD is indispensable.
methodsGene levels were detected via real-time quantitative polymerase chain reaction and western blot. Proliferation, migration and apoptosis were assessed using colony formation assay, wound healing assay, and flow cytometry. Ferroptosis was evaluated through oxidative stress and iron level. Relations between genes were analyzed using Immunoprecipitation (IP) assay and ubiquitination assay, as well as ChIP assay and dual-luciferase reporter assay. USP18 function in vivo was explored using xenograft model.
resultsUbiquitin-specific protease 18 (USP18) was overexpressed in LUAD tissues and cells. LUAD cell proliferation and migration were suppressed but apoptosis and ferroptosis were enhanced after USP18 knockdown. Pou domain, class 4, transcription factor 1 (POU4F1) protein expression was stabilized through USP18-mediated deubiquitination. Function of USP18 silence was reversed by POU4F1 overexpression in LUAD cells. POU4F1 promoted transcription of AMPK-α2 (PRKAA2) and USP18 modulated PRKAA2 protein level via affecting POU4F1. POU4F1 regulated LUAD cell behaviors by upregulating PRKAA2. USP18 enhanced tumor growth in vivo via mediating POU4F1 and PRKAA2.
conclusionAll data demonstrated that USP18 acted as an oncogene in LUAD via interacting with POU4F1/PRKAA2 axis.
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