ArticleProteome science2012
A comparative proteomic study identified LRPPRC and MCM7 as putative actors in imatinib mesylate cross-resistance in Lucena cell line.
Article in Proteome science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- LRPPRC: A Multifunctional Protein Involved in Energy Metabolism and Human Disease.Frontiers in physiology · 2019Pooled it
- Targeting the miR-34a/LRPPRC/MDR1 axis collapse the chemoresistance in P53 inactive colorectal cancer.Cell death and differentiation · 2022Article
- Metabolic Reprogramming During Multidrug Resistance in Leukemias.Frontiers in oncology · 2018Article
- Genetic and epigenetic changes in host ABCB1 influences malaria susceptibility to Plasmodium falciparum.PloS one · 2017Article
- Article
- ABCB1 regulation through LRPPRC is influenced by the methylation status of the GC -100 box in its promoter.Epigenetics · 2014Article
- Proteome Changes Induced by Imatinib and Novel Imatinib Derivatives in K562 Human Chronic Myeloid Leukemia Cells.Proteomes · 2014Article
- Multidrug resistance in chronic myeloid leukaemia: how much can we learn from MDR-CML cell lines?Bioscience reports · 2013Review
- Quantitative- and phospho-proteomic analysis of the yeast response to the tyrosine kinase inhibitor imatinib to pharmacoproteomics-guided drug line extension.Omics : a journal of integrative biology · 2012Article
- Article
- The Biological Role of LRPPRC in Human Cancers.Cancer control : journal of the Moffitt Cancer CenterReview
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough chronic myeloid leukemia (CML) treatment has improved since the introduction of imatinib mesylate (IM), cases of resistance have been reported. This resistance has been associated with the emergence of multidrug resistance (MDR) phenotype, as a BCR-ABL independent mechanism. The classic pathway studied in MDR promotion is ATP-binding cassette (ABC) family transporters expression, but other mechanisms that drive drug resistance are largely unknown. To better understand IM therapy relapse due to the rise of MDR, we compared the proteomic profiles of K562 and Lucena (K562/VCR) cells.
resultsThe use of 2-DE coupled with a MS approach resulted in the identification of 36 differentially expressed proteins. Differential mRNA levels of leucine-rich PPR motif-containing (LRPPRC) protein, minichromosome maintenance complex component 7 (MCM7) and ATP-binding cassette sub-family B (MDR/TAP) member 1 (ABCB1) were capable of defining samples from CML patients as responsive or resistant to therapy.
conclusionsThrough the data presented in this work, we show the relevance of MDR to IM therapy. In addition, our proteomic approach identified candidate actors involved in resistance, which could lead to additional information on BCR-ABL-independent molecular mechanisms.
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Registered trials
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