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Effect of G-rich oligonucleotides on the proliferation of leukemia cells and its relationship with p53 expression

Lei Zhi1, Jianwei Zhang, Yujiao Jia

  • 1State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, People's Republic of China.

Oligonucleotides
|January 21, 2011
PubMed

Insights

G-rich oligonucleotides (GROs) inhibit leukemia cell proliferation by causing S-phase arrest. Introducing the P53 gene reduced GRO effects, suggesting P53 influences GRO uptake and anti-leukemia activity.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • G-rich oligonucleotides (GROs) are known to inhibit tumor cell proliferation via S-phase arrest.
  • GROs interact with cellular proteins like nucleolin, which is linked to P53.
  • The precise relationship between GROs and P53 in leukemia remains unclear.

Purpose of the Study:

  • To investigate the effect of GROs on P53-deficient leukemia cells.
  • To explore the role of P53 in mediating the anti-proliferative effects of GROs.

Main Methods:

  • Treatment of U937 leukemia cells with G-rich oligonucleotides (GROs).
  • Analysis of cell cycle progression and regulatory protein expression.
  • Transfection of U937 cells with a wild-type p53 gene.

Main Results:

  • GROs inhibited U937 cell proliferation and induced S-phase arrest.
  • GROs colocalized with nucleolin in U937 cells, altering cell cycle proteins like Cdk2.
  • P53 gene transfection formed a nucleolin-P53 complex, reducing GROs' anti-leukemia effect, likely by decreasing GRO uptake.

Conclusions:

  • G-rich oligonucleotides effectively inhibit P53-deficient leukemia cell proliferation.
  • The P53 protein plays a role in modulating the cellular response to GROs, potentially by affecting GRO uptake.
  • Targeting the P53-nucleolin interaction could be a strategy for enhancing GRO therapy in leukemia.

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