| Expression pattern: |
UP |
| Associated gene: |
EGFR, PIK3CA |
| Associated microRNA: |
- |
| Biological function: |
CDR1-AS promotes pemetrexed and cisplatin chemoresistance in lung adenocarcinoma; knockdown of CDR1-AS re-sensitizes A549/CR cells to pemetrexed and cisplatin. |
| Molecular mechanism: |
CDR1-AS contributes to pemetrexed and cisplatin chemoresistance through the EGFR/PI3K signaling pathway; activation of EGFR/PI3K mostly restores the effect of CDR1-AS silencing on drug sensitivity. |
| Biological pathway or process: |
EGFR (promotes); drug resistance (promotes); chemoresistance (promotes) |
| Detected method: |
Q
S
|
| Validation methods: |
RNase R Treatment; circRNA-seq; RT-qPCR; Clinical Sample Validation; Transfection; CCK8; Western Blot; Cohort Study; Survival Analysis; Bioinformatics Analysis |
| Clinical significance: |
High CDR1-AS expression is associated with smoking history, T stage and neoadjuvant chemotherapy response, predicts shorter overall survival, and is an independent prognostic biomarker for LUAD patients. |
| Description: |
CDR1-AS is up-regulated in LUAD tissues and cell lines, especially in pemetrexed/cisplatin-insensitive LUAD samples and the resistant A549/CR cell line. High CDR1-AS expression predicts poorer overall survival and functions as an independent prognostic biomarker. Functionally, silencing CDR1-AS re-sensitizes resistant LUAD cells to pemetrexed and cisplatin, while EGFR up-regulation largely reverses this effect, indicating that CDR1-AS promotes chemoresistance through the EGFR/PI3K pathway. |
| Confidence score: |
0.7682 |