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[Effects of DLL4 gene on YY1 and c-Myc protein expression and cell proliferation in leukemia cell line K562]

Li-Fang Shi1, Hong-Bing Rui

  • 1Department of Hematology and Rhematology, Fujian Medical University First Hospital, Fujian Province, China.

Zhongguo Shi Yan Xue Ye Xue Za Zhi
|December 16, 2011
PubMed

Insights

Notch ligand DLL4 enhances transcription factor YY1 and proto-oncogene c-Myc expression in K562 cells. This leads to G(0)/G(1) cell cycle arrest and increased apoptosis, slowing proliferation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • The Notch signaling pathway plays a crucial role in cell development and disease.
  • DLL4 is a key Notch ligand involved in various cellular processes.
  • Understanding DLL4's effects on cancer cells like K562 is important for therapeutic development.

Purpose of the Study:

  • To investigate the impact of Notch ligand DLL4 on K562 cell proliferation.
  • To examine the effects of DLL4 on the protein expression of transcription factor YY1 and proto-oncogene c-Myc.
  • To determine DLL4's influence on cell cycle distribution and apoptosis in K562 cells.

Main Methods:

  • K562 cells were transfected with pBudCE4.1-DLL4 plasmid.
  • Protein expression of DLL4, YY1, and c-Myc was analyzed using Western blot and indirect immunocytochemistry.
  • Cell proliferation was assessed via the CCK-8 assay.
  • Cell cycle and apoptosis were evaluated by flow cytometry.

Main Results:

  • Successful transfection of the DLL4 gene into K562 cells was confirmed.
  • DLL4, YY1, and c-Myc protein levels were significantly elevated in the experimental group.
  • The experimental group showed increased G(0)/G(1) phase cell population and higher apoptosis rates.
  • Cell proliferation was observed to be slower in the DLL4-transfected group.

Conclusions:

  • DLL4 gene transfection upregulates YY1 and c-Myc protein expression in K562 cells.
  • DLL4 induces cell cycle arrest at the G(0)/G(1) phase.
  • DLL4 promotes apoptosis in K562 cells, consequently inhibiting proliferation.

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