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Whole-genome gene expression comparison of the chronic myeloid leukemia cell line K562 and its tyrosine kinase inhibitor resistant subclone K562-IR.

ABSTRACT: Whole-genome gene expression comparison of the chronic myeloid leukemia cell line K562 and its tyrosine kinase inhibitor resistant subclone K562-IR.

PROVIDER: PRJNA495056 | ENA |

REPOSITORIES: ENA

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Whole-genome gene expression comparison of the chronic myeloid leukemia cell line K562 and its tyrosine kinase inhibitor resistant subclone K562-IR.

Project description:The aim of the analysis is to study the relationship between tyrosine kinase inhibitor (TKI) resistance mechanism and phenotypic plasticity in the TKI-resistant and parental chronic myeloid leukemia K562 cell lines, in the presence and absence of imatinib. Results provide insight into the molecular mechanisms underlying the acquisition of cancer cell plasticity.

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Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

Project description:Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

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Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

Project description:Fms-like tyrosine kinase 3 (Flt3) is a regulator of hematopoietic progenitor cells. It is a target of tyrosine kinase inhibitors (TKIs) used for acute myeloid leukemia treatment. Flt3 and its ligand (Flt3L) are expressed in the heart and cardiac side effects occur under Flt3-targeting TKIs. Whether Flt3/Flt3L also regulate cardiac progenitor cells (CPCs), however, is not known. The cardiac side population (SP) is a pool of heterogenous CPCs that can give rise to all cardiac lineages, hence contributing to cardiovascular homeostasis. Here we show that SP-CPCs produce and are responsive to Flt3L. Compared to wild-type, SP-CPCs from flt3L-/- mice are less abundant, with less contribution of CD45-CD34+ cells, and lower expression of gene sets related to epithelial-to-mesenchymal transition, cardiovascular development and stem cell differentiation. Upon culturing and compared to wild-type, flt3L-/- Sca1+CD31- SP-CPCs show increased proliferation and less vasculogenic commitment, but differentiation can be induced in the presence of receptor tyrosine kinase-activating growth factors. The observed differences are associated with decreased microvascularisation and global systolic function of flt3L-/- hearts. Thus, Flt3 contributes to a receptor tyrosine kinase signature necessary for the maintenance and functionality of SP-CPCs. These findings have potential implications regarding cardiovascular side effects observed under TKI therapy.

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