2. Academic Validation
  3. LINC01133 can induce acquired ferroptosis resistance by enhancing the FSP1 mRNA stability through forming the LINC01133-FUS-FSP1 complex

LINC01133 can induce acquired ferroptosis resistance by enhancing the FSP1 mRNA stability through forming the LINC01133-FUS-FSP1 complex

  • Cell Death Dis. 2023 Nov 25;14(11):767. doi: 10.1038/s41419-023-06311-z.
Shaowen Wang 1 2,  Jionghuang Chen 3,  Pengping Li 4,  Yangchao Chen 5 6
Affiliations

Affiliations

  • 1 School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong.
  • 2 Neuromedicine Center, The University of Hong Kong-Shenzhen Hospital, Shenzhen, Guangdong, 518053, China.
  • 3 Department of General Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, 310000, China.
  • 4 Department of Thyroid & Breast Surgery, The First People's Hospital of Xiaoshan District, Xiaoshan Affiliated Hospital of Wenzhou Medical University, Hangzhou, Zhejiang, China.
  • 5 School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong. yangchaochen@cuhk.edu.hk.
  • 6 Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, 518087, China. yangchaochen@cuhk.edu.hk.
PMID: 38007473 DOI: 10.1038/s41419-023-06311-z
Abstract

Due to a lack of research on the critical non-coding RNAs in regulating Ferroptosis, our study aimed to uncover the crucial ones involved in the process. We found that LINC01133 could make pancreatic Cancer cells more resistant to Ferroptosis. A higher expression of LINC01133 was associated with a higher IC50 of sorafenib in clinical samples. Furthermore, we discovered that LINC01133 induced this process through enhancing the mRNA stability of FSP1. CEBPB was the transcription factor to increase the expression of LINC01133. A higher CEBPB could also indicate a higher IC50 of sorafenib in patients with Cancer. Moreover, we confirmed that LINC01133 could form a triple complex with FUS and FSP1 to increase the mRNA stability of FSP1.

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