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Small interfering RNA targeting survivin sensitizes lung cancer cell with mutant p53 to adriamycin

Kimio Yonesaka1, Kenji Tamura, Takayasu Kurata

  • 1Department of Medical Oncology, Kinki University School of Medicine, Osaka-sayama, Osaka, Japan.

International Journal of Cancer
|August 19, 2005
PubMed

Insights

The tumor suppressor p53 downregulates survivin, an apoptosis inhibitor. Inhibiting survivin with siRNA enhances cancer cell sensitivity to adriamycin and promotes apoptosis, offering potential for drug-resistant cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Survivin, an inhibitor of apoptosis protein (IAP), is overexpressed in cancers.
  • p53, a tumor suppressor, induces apoptosis and influences drug sensitivity.
  • The relationship between p53 and survivin in cancer remains to be fully elucidated.

Purpose of the Study:

  • To investigate the regulation of survivin expression by p53 in lung cancer cells.
  • To determine the effect of survivin inhibition on adriamycin sensitivity and apoptosis.
  • To explore the potential of survivin inhibition as a therapeutic strategy.

Main Methods:

  • Examined survivin mRNA and protein levels in lung cancer cell lines with varying p53 status after adriamycin treatment.
  • Utilized small interfering RNA (siRNA) to inhibit p53 and survivin expression.
  • Assessed cell proliferation, apoptosis (TUNEL assay), and pro-caspase3 expression.

Main Results:

  • Wild-type p53 induction led to decreased survivin levels; mutated or null p53 did not show this reduction.
  • p53 inhibition upregulated survivin, while survivin inhibition depressed proliferation in p53-mutated cells.
  • Combined adriamycin and survivin siRNA treatment significantly increased apoptosis and decreased proliferation.

Conclusions:

  • p53 actively downregulates survivin expression.
  • Survivin inhibition enhances cancer cell sensitivity to adriamycin and promotes apoptosis.
  • Targeting survivin with siRNA may improve anticancer drug efficacy, particularly in p53-mutated, drug-resistant cancers.

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