ArticleCell cycle (Georgetown, Tex.)2012
The PERK-eIF2α phosphorylation arm is a pro-survival pathway of BCR-ABL signaling and confers resistance to imatinib treatment in chronic myeloid leukemia cells.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 71 citations in OpenAlex.
- Cell surface GRP78 and the UPR pathway as novel promising therapeutic targets in cancer: an insight into the treatment of acute leukemia by using GRP78-CART cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Article
- 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
- Transcriptional readthrough precedes alternative splicing programs triggered in CML cells by imatinib.Science advances · 2026Article
- The PERK signaling pathway as a marker of the unfolded protein response in patients with acute myeloid leukemia.Turkish journal of medical sciences · 2026Article
- Hypoxia-triggered autophagy modulates cisplatin resistance in non-small cell lung Cancer via EIF2AK3-dependent PI3K/AKT signaling and mTOR-independent mechanisms.Cell death discovery · 2025Article
- Targeting the unfolded protein response in cancer: exploiting endoplasmic reticulum stress for therapeutic intervention.Biochemical pharmacology · 2025Review
- Transcriptional readthrough precedes alternative splicing programs triggered in CML cells by imatinib.bioRxiv : the preprint server for biology · 2025Article
- IL-1β priming triggers an adaptive stress response that enhances pancreatic β-cell resilience to subsequent cytotoxic inflammatory insult.Cell death & disease · 2025Article
- The PERK/ATF4 pathway is required for metabolic reprogramming and progressive lung fibrosis.JCI insight · 2025Article
- Endoplasmic reticulum stress in diseases.MedComm · 2024Review
- NCellular and molecular life sciences : CMLS · 2024Review
- Sublethal engagement of apoptotic pathways in residual cancer.Trends in cell biology · 2024Review
- Protein-rich foods, sea foods, and gut microbiota amplify immune responses in chronic diseases and cancers - Targeting PERK as a novel therapeutic strategy for chronic inflammatory diseases, neurodegenerative disorders, and cancer.Pharmacology & therapeutics · 2024Review
- Targeting PERK-ATF4-P21 axis enhances the sensitivity of osteosarcoma HOS cells to Mppα-PDT.Aging · 2024Article
- Multiple roles for AU-rich RNA binding proteins in the development of haematologic malignancies and their resistance to chemotherapy.RNA biology · 2024Review
- Article
- TIAR and FMRP shape pro-survival nascent proteome of leukemia cells in the bone marrow microenvironment.iScience · 2023Article
- Article
- Targeting the integrated stress response in hematologic malignancies.Experimental hematology & oncology · 2022Review
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Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of adaptive mechanisms plays a crucial role in cancer progression and drug resistance by allowing cell survival under stressful conditions. Therefore, inhibition of the adaptive response is considered as a prospective therapeutic strategy. The PERK-eIF2α phosphorylation pathway is an important arm of the unfolded protein response (UPR), which is induced under conditions of endoplasmic reticulum (ER) stress. Our previous work showed that ER stress is induced in chronic myeloid leukemia (CML) cells. Herein, we demonstrate that the PERK-eIF2α phosphorylation pathway is upregulated in CML cell lines and CD34+ cells from CML patients and is associated with CML progression and imatinib resistance. We also show that induction of apoptosis by imatinib results in the downregulation of the PERK-eIF2α phosphorylation arm. Furthermore, we demonstrate that inactivation of the PERK-eIF2α phosphorylation arm decreases the clonogenic and proliferative capacities of CML cells and sensitizes them to death by imatinib. These findings provide evidence for a pro-survival role of PERK-eIF2α phosphorylation arm that contributes to CML progression and development of imatinib resistance. Thus, the PERK-eIF2α phosphorylation arm may represent a suitable target for therapeutic intervention for CML disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.