ArticleCancer gene therapy2024
CircPKN2 promotes ferroptosis in bladder cancer by promoting the ubiquitination of Stearoyl-CoA Desaturase 1.
Article in Cancer gene therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Stearoyl-CoA desaturase 1 integrates tissue-specific oncogenic pathways into a pan-cancer ferroptosis resistance program.Cell death & disease · 2026Review
- Targeting USP10/SCD1 axis by RAF265 suppresses lipogenesis and induced ferroptosis in head and neck squamous cell carcinoma.Cell death discovery · 2026Article
- Lacylation of Stearoyl-CoA Desaturase-1 Contributes to the Myocardial Ischemia-Reperfusion Injury Through Regulating Wnt/β-Catenin Signaling.Journal of cardiovascular translational research · 2026Article
- The role of ubiquitination and deubiquitination in urological tumours.Frontiers in pharmacology · 2025Review
- Significance of circular RNAs in regulating protein ubiquitination for malignant tumor progression.Frontiers in immunology · 2025Review
- Critical role of non-coding RNA-mediated ferroptosis in urologic malignancies.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
Bladder cancer (BC) is one of the most common malignancies in the male urinary system and currently lacks an optimal treatment strategy. To elucidate the pathogenic mechanisms of BC from the perspective of circular RNAs, we conducted this study. Building upon our previous research, a novel circRNA, circPKN2, captured our interest due to its significant downregulation in BC, and its close association with the prognosis of BC patients. Our research findings indicate that circPKN2 can inhibit the proliferation and migration of BC cells in vitro. Furthermore, we discovered that circPKN2 exerts its anti-cancer effects in BC by promoting ferroptosis. Mechanistic studies revealed that circPKN2 recruits STUB1 to facilitate the ubiquitination of SCD1, thereby suppressing the WNT pathway and promoting ferroptosis in BC. Additionally, our research unveiled the regulatory role of the splicing factor QKI in the biogenesis of circPKN2. Animal studies demonstrated that circPKN2 enhances ferroptosis in BC cells in vivo, inhibiting tumor growth and metastasis. The discovery of the anti-cancer factor circPKN2 holds promise for providing new therapeutic targets in the prevention and treatment of BC.
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