ArticleOncotarget2016
Overexpression of RPS27a contributes to enhanced chemoresistance of CML cells to imatinib by the transactivated STAT3.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Network Pharmacology & Validation of Dihydrotanshinone I's Regulation of HIF-1α via STAT3 in Cardiomyocytes.Acta Cardiologica Sinica · 2026Article
- ZFAS1/STAT3 axis modulates imatinib resistance of chronic myeloid leukemia cells through glucose metabolism reprogramming.Frontiers in oncology · 2025Article
- The Potential Value of RPS27A in Prognosis and Immunotherapy: From Pan-Cancer Analysis to Hepatocellular Carcinoma Validation.ImmunoTargets and therapy · 2024Article
- Comprehensive analysis of mEpigenetics · 2023Article
- In Vivo Investigation of the Effect of Dietary Acrylamide and Evaluation of Its Clinical Relevance in Colon Cancer.Toxics · 2023Article
- Mitochondrial Ribosomal Protein L14 Promotes Cell Growth and Invasion by Modulating Reactive Oxygen Species in Thyroid Cancer.Clinical and experimental otorhinolaryngology · 2023Article
- Case Report: Molecular and microenvironment change upon midostaurin treatment in mast cell leukemia at single-cell level.Frontiers in immunology · 2023Article
- Ribosome Biogenesis: A Central Player in Cancer Metastasis and Therapeutic Resistance.Cancer research · 2022Review
- Comprehensive analysis and validation of novel immune and vascular remodeling related genes signature associated with drug interactions in pulmonary arterial hypertension.Frontiers in genetics · 2022Article
- Silver Nanoparticles Derived byInternational journal of molecular sciences · 2021Article
- Article
- Biological Mechanisms Induced by Soybean Agglutinin Using an Intestinal Cell Model of Monogastric Animals.Frontiers in veterinary science · 2021Article
- Digital microfluidic isolation of single cells for -Omics.Nature communications · 2020Article
- Histone deacetylase inhibitors induce proteolysis of activated CDC42-associated kinase-1 in leukemic cells.Journal of cancer research and clinical oncology · 2016Article
- Decreased expression of LncRNA SLC25A25-AS1 promotes proliferation, chemoresistance, and EMT in colorectal cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STAT3 plays a pivotal role in the hematopoietic system, which constitutively activated by BCR-ABL via JAK and Erk/MAP-kinase pathways. Phospho-STAT3 was overexpressed in imatinib-resistant CML patients as relative to imatinib responsive ones. By activation of the STAT3 pathway, BCR-ABL can promote cell cycling, and inhibit differentiation and apoptosis. Ribosomal protein S27a (RPS27a) performs extra-ribosomal functions besides imparting a role in ribosome biogenesis and post-translational modifications of proteins. RPS27a can promote proliferation, regulate cell cycle progression and inhibit apoptosis of leukemia cells. However, the relationship between STAT3 and RPS27a has not been reported. In this study, we detected a significantly increased expression of STAT3 and RPS27a in bone marrow samples from CML-AP/BP patients compared with those from CML-CP. In addition, we also demonstrated that it was a positive correlation between the level of STAT3 and that of RPS27a. Imatinib-resistant K562/G01 cells expressed significantly higher levels of STAT3 and RPS27a compared with those of K562 cells. RPS27a could be transactivated by p-STAT3 through the specific p-STAT3-binding site located nt -633 to -625 and -486 to -478 of the RPS27a gene promoter in a dose-dependent manner. The transactivated RPS27a could decrease the percentage of apoptotic CML cells induced by imatinib. And the effect of STAT3 overexpression could be counteracted by the p-STAT3 inhibitor WP1066 or RPS27a knockdown. These results suggest that drugs targeting STAT3/p-STAT3/RPS27a combining with TKI might represent a novel therapy strategy in patients with TKI-resistant CML.
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