| Accession |
PRJNA688205 |
| Title |
Long non-coding RNA CRNDE Involved in Resistance to EGFR tyrosine kinase inhibitor in EGFR-mutant Lung Cancer via eIF4A3/MUC1/EGFR Signal. |
| Relevance |
Medical |
| Data types |
Transcriptome or Gene expression |
| Sample scope |
Multiisolate |
| Organism |
Homo sapiens [Taxonomy ID: 9606]
|
| Description |
Introduction: Overcoming of acquired resistance to EGFR-tyrosine kinase inhibitors (EGFR-TKIs) is an intractable obstacle for many clinical oncologists. The mechanisms of resistance to EGFR-TKIs are very complex. Long non-coding RNAs (lncRNAs) may play an important role in cancer development and metastasis. However, the biological process between lncRNAs and drug resistance to EGFR mutated lung cancer largely unknown.
Methods: Osimertinib and afatinib-resistant EGFR-mutated lung cancer cells were established using by a stepwise method. Microarray analysis of non-coding and coding RNAs was performed using parental and resistant EGFR-mutant NSCLC cells.
Results: Microarray analysis was evaluated by bioinformatics analysis through medical-industrial collaboration. CRNDE and DGCR5 lncRNAs were highly expressed in EGFR-TKIs-resistant cells. CRNDE binds to eIF4A3 protein, down-regulates eIF4A3 and MUC1 expression, and down-regulates p-EGFR expression. CRNDE inhibition activated the eIF4A3/MUC1/EGFR signaling pathway and apoptotic activity and restored sensitivity to EGFR-TKIs.
Conclusions: We identified lncRNA CRNDE associated with resistance to EGFR-TKIs in EGFR-mutant NSCLC cells. CRNDE may be a novel therapeutic target for EGFR mutant NSCLC patients.
Overall design: We performed the microarray analysis of non-coding and coding RNAs using parental and resistant EGFR-mutant cell lines. |
| Publication |
| PubMed ID |
Article title |
Journal name |
DOI |
Year |
| 33924522
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| External link |
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| Organization |
Department of Pulmonary Medicine and Oncology,, Nippon Medical School |
| Data Source |
NCBI |
