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Status |
Public on Aug 15, 2024 |
Title |
Molecular mechanisms of BCAT1 in ASK120067-resistant NSCLC cells |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
To investigate the mechanism of BCAT1 in mediating resistance to third-generation EGFR-TKI, we employed RNA-seq analysis to compare the transcriptome signature of ASK120067-resistant NSCLC cells with or without BCAT1 knockdown. Here, gene set enrichment (GSEA) revealed a significant decrease in the expression of genes in glycolysis pathway following small interfering RNA (siRNA)-mediated BCAT1 knockdown, which indicated the role for BCAT1 in supporting TKI resistance through upregulation of glycolysis.
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Overall design |
Total mRNA profiles of 67R (ASK120067-resistant NCI-H1975) cells with and without BCAT1 knockdown.
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Contributor(s) |
Zhang T, Pan Z, Xie H |
Citation(s) |
39143065 |
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Submission date |
Nov 13, 2023 |
Last update date |
Aug 15, 2024 |
Contact name |
Zilu Pan |
E-mail(s) |
[email protected]
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Organization name |
Shanghai Institute of Materia Medica
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Street address |
No. 555 Zuchongzhi Road
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City |
Shanghai |
ZIP/Postal code |
201203 |
Country |
China |
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Platforms (1) |
GPL24676 |
Illumina NovaSeq 6000 (Homo sapiens) |
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Samples (6)
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Relations |
BioProject |
PRJNA1039771 |