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Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype
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Published on: June 17, 2022

Genomic c-Myc quadruplex DNA selectively kills leukemia.

Kara C Sedoris1, Shelia D Thomas, Cortney R Clarkson

  • 1Department of Medicine, James Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA.

Molecular Cancer Therapeutics
|November 16, 2011
PubMed
Summary

A novel DNA sequence (PU27) targets the c-Myc oncogene in leukemia, inducing cancer cell death via oncotic necrosis. This approach improves upon traditional oligonucleotide therapies by enhancing cellular uptake and stability while sparing normal cells.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • c-Myc is a critical regulator of cell proliferation, frequently overexpressed in leukemia, correlating with poor patient outcomes.
  • Conventional antisense oligonucleotides targeting c-Myc show limited efficacy due to poor cellular uptake, rapid degradation, and off-target effects on normal cells.

Purpose of the Study:

  • To investigate the biological significance of a guanine-rich quadruplex-forming sequence (PU27) in the c-Myc promoter as a potential therapeutic target.
  • To evaluate the efficacy and safety of a PU27 oligonucleotide in treating leukemia, addressing limitations of current oligonucleotide therapies.

Main Methods:

  • Treatment of leukemia cells with a PU27 oligonucleotide designed to form DNA quadruplexes.
  • Assessment of c-Myc mRNA and protein expression levels.
  • Evaluation of cellular effects including cell-cycle arrest, oncotic necrosis, DNA damage, mitochondrial function, ATP levels, and oxidative stress.
  • Analysis of PU27 cellular uptake, stability, and effects on normal cells.

Main Results:

  • PU27 oligonucleotide treatment effectively suppressed c-Myc expression, leading to cell-cycle arrest and oncotic necrosis in leukemia cells.
  • PU27 demonstrated excellent cellular uptake, stability in serum and intracellularly, and showed no adverse effects on normal cells.
  • Suppression of c-Myc by PU27 induced DNA damage, cellular and mitochondrial swelling, and membrane permeability, characteristic of oncotic necrosis, along with mitochondrial dysfunction and ATP depletion.

Conclusions:

  • The PU27 oligonucleotide represents a novel and effective therapeutic strategy for leukemia by selectively inducing oncotic necrosis through c-Myc suppression.
  • This approach overcomes key challenges associated with oligonucleotide therapeutics, including cellular uptake, stability, and specificity, offering a promising new avenue for cancer treatment.