Gene expression profile of circulating CD34+ cells and granulocytes in chronic myeloid leukemia

Čokić, Vladan P.; Mojsilović, Slavko; Jauković, Aleksandra; Kraguljac-Kurtovic, Nada; Mojsilović, Sonja; Šefer, Dragan; Ajtić, Olivera Mitrović; Milosevic, Violeta; Bogdanović, Andrija; Đikić, Dragoslava; Milenković, P; Puri, Raj K.

doi:10.1016/j.bcmd.2015.08.002

Cited by 12 publications

(7 citation statements)

References 18 publications

(34 reference statements)

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“… 37 SERBP1 has been found to be significantly upregulated in CD34+ CML cases compared with control C34+ cells. 38 Significant hypermethylation of the YBX3 promoter to downregulate its mRNA expression has been found in AML. 39 HNRNPM has been found to promote cancer metastasis by regulating alternative splicing.…”

Section: Discussionmentioning

confidence: 99%

Mutant JAK3 phosphoproteomic profiling predicts synergism between JAK3 inhibitors and MEK/BCL2 inhibitors for the treatment of T-cell acute lymphoblastic leukemia

et al. 2017

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Mutations in the interleukin-7 receptor (IL7R) or the Janus kinase 3 (JAK3) kinase occur frequently in T-cell acute lymphoblastic leukemia (T-ALL) and both are able to drive cellular transformation and the development of T-ALL in mouse models. However, the signal transduction pathways downstream of JAK3 mutations remain poorly characterized. Here we describe the phosphoproteome downstream of the JAK3(L857Q)/(M511I) activating mutations in transformed Ba/F3 lymphocyte cells. Signaling pathways regulated by JAK3 mutants were assessed following acute inhibition of JAK1/JAK3 using the JAK kinase inhibitors ruxolitinib or tofacitinib. Comprehensive network interrogation using the phosphoproteomic signatures identified significant changes in pathways regulating cell cycle, translation initiation, mitogen-activated protein kinase and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT signaling, RNA metabolism, as well as epigenetic and apoptotic processes. Key regulatory proteins within pathways that showed altered phosphorylation following JAK inhibition were targeted using selumetinib and trametinib (MEK), buparlisib (PI3K) and ABT-199 (BCL2), and found to be synergistic in combination with JAK kinase inhibitors in primary T-ALL samples harboring JAK3 mutations. These data provide the first detailed molecular characterization of the downstream signaling pathways regulated by JAK3 mutations and provide further understanding into the oncogenic processes regulated by constitutive kinase activation aiding in the development of improved combinatorial treatment regimens.

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Section: Discussionmentioning

confidence: 99%

Mutant JAK3 phosphoproteomic profiling predicts synergism between JAK3 inhibitors and MEK/BCL2 inhibitors for the treatment of T-cell acute lymphoblastic leukemia

et al. 2017

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“…The PI3K signaling pathway is important in maintaining normal stem cells and CML LSCs. One study reported PI3K signaling upregulates in CML LSCs [74] and correlates with P210 BCRABL1 levels [75]. Normally, AKT phosphorylates FOXO transcription factors where it is sequestered in the cytoplasm.…”

Section: Effects Of Signaling Pathways On CML Lscsmentioning

confidence: 99%

Chronic myeloid leukemia stem cells

et al. 2019

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Chronic myeloid leukemia (CML) is caused by BCRABL1 in a cell with the biological potential, intrinsic or acquired, to cause leukemia. This cell is commonly termed the CML leukemia stem cell (LSC). In humans a CML LSC is operationally-defined by ≥1 in vitro or in vivo assays of human leukemia cells transferred to immune-deficient mice. Results of these assays are sometimes discordant. There is also the unproved assumption that biological features of a CML LSC are stable. These considerations make accurate and precise identification of a CML LSC difficult or impossible. In this review, we consider biological features of CML LSCs defined by these assays. We also consider whether CML LSCs are susceptible to targeting by tyrosine kinase inhibitors (TKIs) and other drugs, and whether elimination of CML LSCs is needed to achieve therapy-free remission or cure CML.

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“…LGALS16 was also recognized as a brain tissue-specific gene within genome-wide associations with several neuroimaging psychiatric traits [ 61 ]. Further, LGALS16 was expressed two-fold higher in chronic myeloid leukemia granulocytes compared to controls [ 62 ]. Copy number variations were identified in chromosome 19 for multiple genes including LGALS16 in association with clinical features, such as histological type, ethnicity, disease stage, and familial history, of breast cancer using tumor samples from a Brazilian cohort [ 63 ].…”

Section: Resultsmentioning

confidence: 99%

Expression, Regulation, and Functions of the Galectin-16 Gene in Human Cells and Tissues

Kaminker

Timoshenko

2021

Biomolecules

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Galectins comprise a family of soluble β-galactoside-binding proteins, which regulate a variety of key biological processes including cell growth, differentiation, survival, and death. This paper aims to address the current knowledge on the unique properties, regulation, and expression of the galectin-16 gene (LGALS16) in human cells and tissues. To date, there are limited studies on this galectin, with most focusing on its tissue specificity to the placenta. Here, we report the expression and 8-Br-cAMP-induced upregulation of LGALS16 in two placental cell lines (BeWo and JEG-3) in the context of trophoblastic differentiation. In addition, we provide the results of a bioinformatics search for LGALS16 using datasets available at GEO, Human Protein Atlas, and prediction tools for relevant transcription factors and miRNAs. Our findings indicate that LGALS16 is detected by microarrays in diverse human cells/tissues and alters expression in association with cancer, diabetes, and brain diseases. Molecular mechanisms of the transcriptional and post-transcriptional regulation of LGALS16 are also discussed based on the available bioinformatics resources.

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Gene expression profile of circulating CD34+ cells and granulocytes in chronic myeloid leukemia

Cited by 12 publications

References 18 publications

Mutant JAK3 phosphoproteomic profiling predicts synergism between JAK3 inhibitors and MEK/BCL2 inhibitors for the treatment of T-cell acute lymphoblastic leukemia

Mutant JAK3 phosphoproteomic profiling predicts synergism between JAK3 inhibitors and MEK/BCL2 inhibitors for the treatment of T-cell acute lymphoblastic leukemia

Chronic myeloid leukemia stem cells

Expression, Regulation, and Functions of the Galectin-16 Gene in Human Cells and Tissues

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