ArticleInternational journal of molecular medicine2012
Alternative splicing of apoptosis-related genes in imatinib-treated K562 cells identified by exon array analysis.
Article in International journal of molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 23 citations in OpenAlex.
- TIAR-dependent coordination of alternative splicing and lipid peroxidation is required for CML cell resistance to imatinib in the bone marrow stroma.bioRxiv : the preprint server for biology · 2026Article
- System Prediction and Validation of TCM for Chronic Myeloid Leukemia Treatment from the Perspective of Low-Toxicity Chemotherapy: A StilbeneEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Differentially expressed alternatively spliced genes in skeletal muscle from cancer patients with cachexia.Journal of cachexia, sarcopenia and muscle · 2018Article
- Genome-wide Profiling of RNA splicing in prostate tumor from RNA-seq data using virtual microarrays.Journal of clinical bioinformatics · 2012Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imatinib is the therapeutic standard for newly diagnosed patients with chronic myeloid leukemia (CML). In these patients, imatinib has been shown to induce an apoptotic response specifically in cells expressing the oncogenic fusion protein BCR-ABL. Previous studies in our lab revealed that imatinib-induced apoptosis in K562 cells involves a shift in production of Bcl-x splice isoforms towards the pro-apoptotic Bcl-xs splice variant. Here, we report the findings from our subsequent study to identify other apoptosis-related genes that are differentially spliced in response to imatinib treatment. Gene expression profiling of imatinib-treated K562 cells was performed by the Affymetrix GeneChip Human Exon 1.0 ST array, and differences in exon-level expression and alternative splicing were analyzed using the easyExon software. Detailed analysis by reverse transcription-PCR (RT-PCR) and sequencing of key genes confirmed the experimental results of the exon array. Our results suggest that imatinib treatment of K562 cells causes a transcriptional shift towards alternative splicing in a large number of apoptotic genes. The present study provides insight into the molecular character of apoptotic leukemia cells and may help to improve the mechanism of imatinib therapy in patients with CML.
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