| Expression pattern: |
UP |
| Associated gene: |
NRF2, BCLAF1, SLC7A11, Myc |
| Associated microRNA: |
- |
| Biological function: |
cDTL promotes breast cancer cell growth and tumor progression by limiting ferroptosis; cDTL knockdown inhibits breast cancer cell viability, colony formation and in vivo tumor growth through promoting ferroptosis. |
| Molecular mechanism: |
cDTL acts through direct protein binding: nuclear cDTL binds NRF2 to increase SLC7A11 transcription, while cytoplasmic cDTL binds BCLAF1 to stabilize SLC7A11 mRNA, activating the SLC7A11/GSH/GPX4 axis and repressing ferroptosis; cDTL is transcriptionally activated by Myc. |
| Biological pathway or process: |
ferroptosis (inhibits); proliferation (promotes); mRNA stability (promotes); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; RNase R Treatment; FISH / smFISH; Clinical Sample Validation; RIP (RNA Immunoprecipitation); RNA Pull-Down; ChIP / ChIP-seq; Luciferase Reporter Assay; Transfection; CCK8; Colony Formation Assay; In Vivo Animal Model; Western Blot; Cohort Study; Survival Analysis; Bioinformatics Analysis |
| Clinical significance: |
cDTL was overexpressed in human breast cancer tissues and was associated with shorter progression-free survival time and poor differentiation; it may be a potential therapeutic target for breast cancer. |
| Description: |
cDTL is an up-regulated DTL-derived circular RNA in breast cancer that supports tumor cell growth by suppressing ferroptosis. Mechanistically, cDTL binds NRF2 in the nucleus to enhance SLC7A11 transcription and binds BCLAF1 in the cytoplasm to stabilize SLC7A11 mRNA, thereby activating the SLC7A11/GSH/GPX4 ferroptosis-resistance axis. High cDTL expression is associated with shorter progression-free survival and poor differentiation, suggesting therapeutic relevance. |
| Confidence score: |
0.8536 |