Assay of OAZ1 mRNA Levels in Chronic Myeloid Leukemia Combined with Application of Leukemia PCR Array Identified Relevant Gene Changes Affected by Antizyme

Wu, Bingping; Wang, Xing; Ma, Wenxue; Wen-ling, Zheng; Jiang, Li

doi:10.1159/000353406

Cited by 6 publications

(6 citation statements)

References 36 publications

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“…The naturally occurring ODC antienzymes (OAZ1, OAZ2, and OAZ3) negatively regulate ODC activity in response to elevated intracellular polyamine levels. However, analysis of the mRNA levels of OAZ1 in some leukemias points to a significant downregulation in its expression ( 99 ). Alternative strategies for inhibiting ODC activity in cancer cells have been explored.…”

Section: Conditionally Essential Amino Acidsmentioning

confidence: 99%

Targeting Amino Acid Metabolic Vulnerabilities in Myeloid Malignancies

et al. 2021

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Tumor cells require a higher supply of nutrients for growth and proliferation than normal cells. It is well established that metabolic reprograming in cancers for increased nutrient supply exposes a host of targetable vulnerabilities. In this article we review the documented changes in expression patterns of amino acid metabolic enzymes and transporters in myeloid malignancies and the growing list of small molecules and therapeutic strategies used to disrupt amino acid metabolic circuits within the cell. Pharmacological inhibition of amino acid metabolism is effective in inducing cell death in leukemic stem cells and primary blasts, as well as in reducing tumor burden in in vivo murine models of human disease. Thus targeting amino acid metabolism provides a host of potential translational opportunities for exploitation to improve the outcomes for patients with myeloid malignancies.

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Section: Conditionally Essential Amino Acidsmentioning

confidence: 99%

Targeting Amino Acid Metabolic Vulnerabilities in Myeloid Malignancies

et al. 2021

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“…On the other hand, AML cells often constitutively produce CXCL10, with wide variations between patients potentially reflecting disease status [74]. Considering chronic myeloid leukemia (CML), a fourth leukemic subtype, CXCL10 mRNA levels were just recently reported to be upregulated in peripheral blood mononuclear cells isolated from CML patients, linking CXCR3 ligands to the pathogenesis of CML as well [75]. Dysregulation of CXCL10 gene expression has in fact been associated with several recurrent chromosomal translocations identified in different leukemic pathologies [76].…”

Section: Leukemia Lymphoma and Myelomamentioning

confidence: 99%

CXCR3 ligands in disease and therapy

Raemdonck

Steen

Liekens

et al. 2015

Cytokine & Growth Factor Reviews

268

205

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Chemokines, binding their various G protein-coupled receptors, lead the way for leukocytes in health and inflammation. Yet chemokine receptor expression is not limited to leukocytes. Accordingly, chemokines are remarkably pleiotropic molecules involved in a range of physiological as well as pathological processes. For example, the CXCR3 chemokine receptor is expressed on activated T lymphocytes, dendritic cells and natural killer cells, but also fibroblasts and smooth muscle, epithelial and endothelial cells. In men, these cells express either CXCR3A, its splice variant CXCR3B or a balanced combination of both. The CXCR3 ligands, activating both receptor variants, include CXCL4, CXCL4L1, CXCL9, CXCL10 and CXCL11. Upon CXCR3A activation these ELR-negative CXC chemokines mediate chemotactic and proliferative responses, for example in leukocytes. In contrast, CXCR3B induces anti-proliferative and anti-migratory effects, as exemplified by angiostatic effects on endothelial cells. Taken together, the unusual and versatile characteristics of CXCR3 and its ligands form the basis for their pertinent involvement in a myriad of diseases. In this review, we discuss the presence and function of all CXCR3 ligands in various malignant, angiogenic, infectious, inflammatory and other disorders. By extension, we have also elaborated on the potential therapeutic applicability of CXCR3 ligand administration or blockade, as well as their additional value as predictive or prognostic biomarkers. This review illustrates the multifunctional, intriguing character of the various CXCR3-binding chemokines.

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“…Ornithine decarboxylase antizyme ( OAZ1 gene) is a potential therapeutic target in various malignant tumors because it plays relevant roles in cellular functions, including genomic stability, proliferation, differentiation, and apoptosis [ 42 ]. The enhancer-related lncRNA-mRNA pairs as prognostic biomarkers AC0-27307.2- OAZ1 in the Basal-like subtype of breast cancer [ 43 ] and as a fusion gene.…”

Section: Discussionmentioning

confidence: 99%

Deep Learning Techniques to Characterize the RPS28P7 Pseudogene and the Metazoa-SRP Gene as Drug Potential Targets in Pancreatic Cancer Patients

Salgado,

Prado Montes de Oca,

Chairez

et al. 2024

Biomedicines

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The molecular explanation about why some pancreatic cancer (PaCa) patients die early and others die later is poorly understood. This study aimed to discover potential novel markers and drug targets that could be useful to stratify and extend expected survival in prospective early-death patients. We deployed a deep learning algorithm and analyzed the gene copy number, gene expression, and protein expression data of death versus alive PaCa patients from the GDC cohort. The genes with higher relative amplification (copy number >4 times in the dead compared with the alive group) were EWSR1, FLT3, GPC3, HIF1A, HLF, and MEN1. The most highly up-regulated genes (>8.5-fold change) in the death group were RPL30, RPL37, RPS28P7, RPS11, Metazoa_SRP, CAPNS1, FN1, H3−3B, LCN2, and OAZ1. None of their corresponding proteins were up or down-regulated in the death group. The mRNA of the RPS28P7 pseudogene could act as ceRNA sponging the miRNA that was originally directed to the parental gene RPS28. We propose RPS28P7 mRNA as the most druggable target that can be modulated with small molecules or the RNA technology approach. These markers could be added as criteria to patient stratification in future PaCa drug trials, but further validation in the target populations is encouraged.

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Assay of OAZ1 mRNA Levels in Chronic Myeloid Leukemia Combined with Application of Leukemia PCR Array Identified Relevant Gene Changes Affected by Antizyme

Cited by 6 publications

References 36 publications

Targeting Amino Acid Metabolic Vulnerabilities in Myeloid Malignancies

Targeting Amino Acid Metabolic Vulnerabilities in Myeloid Malignancies

CXCR3 ligands in disease and therapy

Deep Learning Techniques to Characterize the RPS28P7 Pseudogene and the Metazoa-SRP Gene as Drug Potential Targets in Pancreatic Cancer Patients

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