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| Status |
Public on Apr 13, 2024 |
| Title |
Whole transcriptome sequencing for wild type and IRAIN over-expression K562 cells |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
The development of tyrosine kinase inhibitors (TKIs) has revolutionarily increased the overall survival of patients with chronic myeloid leukemia (CML). However, drug resistance remains a major obstacle. Here, we demonstrated that a BCR-ABL1-independent long non-coding RNA, IRAIN, is constitutively expressed at low levels in CML, resulting in imatinib resistance. IRAIN knockdown decreased the sensitivity of CD34+ CML blasts and cell lines to imatinib, whereas IRAIN overexpression significantly increased sensitivity. Mechanistically, IRAIN downregulates CD44, a membrane receptor favorably affecting TKI resistance, by binding to the nuclear factor kappa B subunit p65 to reduce the expression of p65 and phosphorylated p65. Therefore, the demethylating drug decitabine, which upregulates IRAIN, combined with imatinib, formed a dual therapy strategy which can be applied to CML with resistance to TKIs.
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| Overall design |
Investigation of drug resistance for over-expression IRAIN1 in CML cell line K562
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| Citation(s) |
38784023 |
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| Submission date |
Apr 10, 2024 |
| Last update date |
Jun 05, 2024 |
| Contact name |
Jinsong Yan |
| E-mail(s) |
[email protected]
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| Organization name |
Dalian Medical University
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| Department |
Institute of Cancer Stem Cell
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| Street address |
9 west section, Lvshun south road, Dalian, Liaoning Province, China
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| City |
Dalian |
| ZIP/Postal code |
116044 |
| 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 |
PRJNA1098625 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE263645_Counts.xlsx |
3.7 Mb |
(ftp)(http) |
XLSX |
SRA Run Selector |
| Raw data are available in SRA |
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