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LUCAT1 inhibits ferroptosis in bladder cancer by regulating the mRNA stability of STAT3.
Cao, Yuepeng; Zou, Zhuo; Wu, Xuhong; Li, Weijian; Lu, Zhen; Hu, Jiawei; Yang, Liu.
Afiliación
  • Cao Y; Department of Colorectal Surgery, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing, China. Electronic address: MF1535001@smail.nju.edu.cn.
  • Zou Z; Graduate School, Dalian Medical University, Dalian, China.
  • Wu X; Department of Critical Care Medicine, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing, China.
  • Li W; Department of Urology, Northern Jiangsu People's Hospital, Clinical Medical College of Yangzhou University, Yangzhou, China.
  • Lu Z; Department of Anesthesiology, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing, China. Electronic address: luzhen120@Sohu.com.
  • Hu J; Department of Endoscopy, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing, China.
  • Yang L; Department of Colorectal Surgery, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing, China. Electronic address: yangliu@njmu.edu.cn.
Gene ; 894: 147974, 2024 Feb 05.
Article en En | MEDLINE | ID: mdl-37944649
OBJECT: In this study, we aimed to elucidate the role of LUCAT1, a recently identified lncRNA, in ferroptosis within the context of bladder cancer (BC). METHODS: Through a comprehensive array of experimental techniques, including transmission electron microscopy (TEM), RNA pull-down assays, and fluorescence in situ hybridization (FISH), we investigated the molecular interactions and functional consequences associated with LUCAT1 in BC cells. RESULTS: Our findings indicate that LUCAT1 acts as a pivotal regulator in BC, fostering cell proliferation, migration, and invasion, while concurrently impeding ferroptosis. Mechanistically, we unveiled a direct binding between LUCAT1 and insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1), which governs the mRNA stability of signal transducer and activator of transcription 3 (STAT3). Intriguingly, ectopic expression of STAT3 counteracted the suppressive effect of LUCAT1 on ferroptosis induction in BC cells. Notably, in an in vivo setting, LUCAT1 emerged as a crucial modulator of ferroptosis inhibition in BC by regulating STAT3 mRNA stability. CONCLUSION: Collectively, our study identifies LUCAT1 as a novel oncogenic player, repressing ferroptosis in BC. These findings shed light on the intricate interplay between lncRNAs and ferroptosis in cancer, implicating LUCAT1 as a promising therapeutic target for patients afflicted with BC. Further investigations into the underlying mechanisms governing LUCAT1-mediated ferroptosis resistance are warranted, with the potential to uncover novel strategies for combating BC progression and improving patient outcomes.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias de la Vejiga Urinaria / MicroARNs / ARN Largo no Codificante / Ferroptosis Límite: Humans Idioma: En Revista: Gene Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias de la Vejiga Urinaria / MicroARNs / ARN Largo no Codificante / Ferroptosis Límite: Humans Idioma: En Revista: Gene Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos