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[BMMSC from blastic phase CML down-regulate leukemia cell apoptosis].

Ying Wang1, Yu-Xiang Han2, Zhi-Yun Niu1

  • 1Departments of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China.

Zhongguo Shi Yan Xue Ye Xue Za Zhi
|October 24, 2014
PubMed
Summary
This summary is machine-generated.

Bone marrow mesenchymal stem cells (BMMSC) from chronic myeloid leukemia (CML) blastic phase (Bp) patients protect leukemia cells from chemotherapy-induced apoptosis. CML-Bp BMMSC inhibit apoptosis by affecting mitochondrial membrane potential and caspase expression.

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Area of Science:

  • Hematology
  • Stem Cell Biology
  • Cancer Biology

Background:

  • Mesenchymal stem cells (MSCs) play a role in the tumor microenvironment.
  • Chronic myeloid leukemia (CML) in blastic phase (Bp) is an aggressive form of leukemia.
  • Understanding the interaction between CML cells and MSCs is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the effect of bone marrow mesenchymal stem cells (BMMSC) from CML-Bp patients on K562 and primary CML-Bp cells.
  • To explore the underlying mechanisms of this interaction, particularly concerning chemotherapy resistance.

Main Methods:

  • Co-culture of K562 cells and primary CML-Bp cells with BMMSC from different patient groups (CML-Bp, CML-chronic phase (CML-Cp), and normal).
  • Assessment of cell proliferation (MTT assay), apoptosis rate and mitochondrial membrane potential (flow cytometry).
  • Measurement of Caspase-8, Caspase-9, and activated Caspase-3 expression (Western blot).

Main Results:

  • CML-Bp BMMSC enhanced the survival of K562 cells treated with adviamycin (ADM), inhibiting ADM-induced apoptosis.
  • CML-Bp BMMSC exhibited a stronger protective effect on leukemic cells compared to CML-Cp BMMSC and normal BMMSC.
  • Co-culture with CML-Bp BMMSC led to a slight drop in mitochondrial membrane potential and altered caspase expression (down-regulated caspase-3, increased caspase-9).

Conclusions:

  • CML-Bp BMMSC down-regulate chemotherapy-induced apoptosis in leukemia cells.
  • The mechanism involves inhibiting the drop in mitochondrial membrane potential and modulating caspase-9 and caspase-3 expression.
  • These findings suggest CML-Bp BMMSC contribute to chemoresistance in CML-Bp.