Research Progress on TKI Resistance of CML Cells Mediated by MSC through CXCL12/CXCR4 Axis.
10.7534/j.issn.1009-2137.2015.04.062
- Author:
Li-Jun FANG
1
;
Huai-Jun TU
2
;
Jian LI
3
Author Information
1. Key Laboratory of Hematology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China.
2. Department of Neurology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China.
3. Key Laboratory of Hematology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China. E-mail: jeniferjian@gmail.com.
- Publication Type:Journal Article
- MeSH:
Drug Resistance, Neoplasm;
Humans;
Leukemia, Myelogenous, Chronic, BCR-ABL Positive;
Protein Kinase Inhibitors;
Protein-Tyrosine Kinases;
Signal Transduction;
Stem Cells
- From:
Journal of Experimental Hematology
2015;23(4):1221-1224
- CountryChina
- Language:Chinese
-
Abstract:
Although the tyrosinekinase inhibitors (TKI) displayed a significant curative effect on chronic myeloid leukemia (CML), but the drug resistance in treatment course of this disease still can not be avoided. Studies recently have shown that the mesenchymal stem cells (MSC) can induce CML cells to resist TKI therapy by CXCL12/CXCR4 axis from multiple aspects, such as the directional migration of CML cells, adherence to marrow cavity, the mediation of cell protective dormancy, activations of numerous survival signaling pathways, the suppression of mitochondrial-dependent apoptosis and the up-regulated expression of BCL-6. The combination of TKI and CXCR4 antagonists will be a novel treatment strategy to raise the genetic cure rate of CML. In this article, the pathways of drug resistance, pathways of sensitivity to CXCL12 and pathways of CML cell adherence to marrow cavity in CML cells mediated by MSC were reviewed.
