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LINC01133 can induce acquired ferroptosis resistance by enhancing the FSP1 mRNA stability through forming the
Shaowen Wang1,2, Jionghuang Chen3, Pengping Li4
1School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong.
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.
Insights
This study reveals LINC01133 enhances ferroptosis resistance in pancreatic cancer by stabilizing FSP1 mRNA. Higher LINC01133 and CEBPB levels correlate with sorafenib resistance in patients.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Ferroptosis is a critical cell death pathway in cancer therapy.
- Non-coding RNAs play a significant role in regulating cellular processes, including ferroptosis.
- Limited research exists on non-coding RNAs involved in ferroptosis regulation in pancreatic cancer.
Purpose of the Study:
- To identify key non-coding RNAs regulating ferroptosis in pancreatic cancer.
- To elucidate the mechanism by which LINC01133 influences ferroptosis resistance.
- To investigate the clinical relevance of LINC01133 and its associated factors in pancreatic cancer patients.
Main Methods:
- Expression analysis of LINC01133 in pancreatic cancer cells and clinical samples.
- Investigation of LINC01133's effect on ferroptosis sensitivity.
- mRNA stability assays for FSP1.
- Identification of transcription factors regulating LINC01133 expression.
- Analysis of correlations between LINC01133, CEBPB, and sorafenib IC50 values.
Main Results:
- LINC01133 was found to confer resistance to ferroptosis in pancreatic cancer cells.
- Increased LINC01133 expression correlated with higher sorafenib IC50 values in patients.
- LINC01133 enhances FSP1 mRNA stability, contributing to ferroptosis resistance.
- The transcription factor CEBPB increases LINC01133 expression and is associated with sorafenib resistance.
- LINC01133 forms a triple complex with FUS and FSP1 to stabilize FSP1 mRNA.
Conclusions:
- LINC01133 is a crucial regulator of ferroptosis in pancreatic cancer.
- The LINC01133/FSP1 axis represents a potential therapeutic target for overcoming sorafenib resistance.
- CEBPB-mediated upregulation of LINC01133 contributes to treatment resistance in pancreatic cancer.
