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Updated: Jun 12, 2026

Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

[Arresting effect of p16 and dll4 transfection on cell cycle of K562 cells]

Jie-Fang Shen1, Hong-Bing Rui, Jin-Zi Su

  • 1Department of Rheumatology and Hematology, The First Hospital Affiliated to Fujian Medical University, Fuzhou 350004, Fujian Province, China.

Zhongguo Shi Yan Xue Ye Xue Za Zhi
|June 22, 2010
PubMed

Insights

Introducing p16 and delta-like 4 (Dll4) genes into leukemia K562 cells via a recombinant plasmid effectively inhibited cell proliferation. This genetic modification resulted in cell cycle arrest at the G0/G1 phase, offering a potential therapeutic strategy for leukemia.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Context:

  • Leukemia K562 cells are a common model for studying chronic myeloid leukemia.
  • Understanding the role of specific genes in leukemia cell proliferation is crucial for developing targeted therapies.
  • Eukaryotic expression vectors are essential tools for investigating gene function in vitro.

Purpose:

  • To investigate the simultaneous expression and functional role of p16 and DLL4 genes in leukemia K562 cells.
  • To construct and validate a novel eukaryotic expression vector (pBudCE4.1-16-dll4) for co-expressing p16 and DLL4.
  • To assess the impact of p16 and DLL4 co-expression on K562 cell proliferation and cell cycle progression.

Summary:

  • A recombinant plasmid, pBudCE4.1-16-dll4, was successfully constructed and transfected into K562 cells, leading to detectable expression of exogenous P16 and Dll4 proteins.
  • Transfection with the pBudCE4.1-16-dll4 vector induced significant G(0)/G(1) phase arrest in K562 cells.
  • The co-expression of p16 and DLL4 genes resulted in a marked reduction in K562 cell proliferation compared to control groups.

Impact:

  • Demonstrates the feasibility of simultaneous p16 and DLL4 gene expression in leukemia cells using a eukaryotic vector.
  • Provides evidence for the anti-proliferative effects of p16 and DLL4 co-expression, specifically G(0)/G(1) arrest, in K562 cells.
  • Highlights a potential therapeutic strategy for leukemia by targeting cell cycle regulation through combined p16 and DLL4 gene delivery.

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