Bone mesenchymal stromal cells exhibit functional inhibition but no chromosomal aberrations in chronic myelogenous leukemia

Xie,Jieqiong; Chen,Jiadi; Wang,Bin; He,Xuchun; Huang,Huifang

doi:10.3892/ol.2018.9681

Bone mesenchymal stromal cells exhibit functional inhibition but no chromosomal aberrations in chronic myelogenous leukemia

Authors:
- Jieqiong Xie
- Jiadi Chen
- Bin Wang
- Xuchun He
- Huifang Huang
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Affiliations: Central Laboratory, Fujian Provincial Key Laboratory of Hematology, Fujian Medical University Union Hospital, Fuzhou, Fujian 350001, P.R. China, Fujian Institute of Hematology, Fujian Provincial Key Laboratory of Hematology, Fujian Medical University Union Hospital, Fuzhou, Fujian 350001, P.R. China, Department of Medical Technology, Fujian Health Career Technical College, Fuzhou, Fujian 350101, P.R. China
Published online on: November 9, 2018 https://doi.org/10.3892/ol.2018.9681
Pages: 999-1007
Copyright: © Xie et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Chronic myelogenous leukemia (CML) is a myeloproliferative neoplasia characterized by the presence of the Philadelphia (Ph) chromosome in hematopoietic cells (HCs). As one of the most important components of the bone marrow microenvironment (BMM), bone mesenchymal stromal cells (BMSCs) are critical in the development of leukemia and essential in the regulation of hematopoiesis. However, little is known regarding the alterations of BMSCs in CML. The current study performed Cell Counting Kit‑8 and colony‑forming unit fibroblast assays to evaluate the proliferative ability of BMSCs. The percentage of senescent BMSCs was evaluated by a senescence‑associated β‑galactosidase staining assay. Subsequently, a long‑term culture‑initiating cell assay was designed to explore the HC‑supporting capacity of the BMSCs. Furthermore, cytogenetics were detected by conventional cytogenetic analysis and fluorescence in situ hybridization analysis. The current results revealed that CML‑BMSCs exhibited decreased cell proliferation and impaired HC‑support capacity, as well as increased susceptibility to senescence. No chromosomal aberrations, including the absence of the Ph chromosome, were noted in all CML‑BMSCs. In conclusion, the current study demonstrated functional inhibition of CML‑BMSCs; however, no signs of chromosomal aberrations were observed, thereby providing insight into the changes occurring in the CML‑BMM.

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