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Rapamycin decreases survivin expression to induce NSCLC cell apoptosis under hypoxia through inhibiting HIF-1α

Bin Chen1, Sun Yuping, Jian Ni

  • 1Department of Oncology, Shanghai Pulmonary Hospital, Tongji Univeristy School of Medicine, Shanghai, 200433, People's Republic of China.

Molecular Biology Reports
|May 14, 2011
PubMed

Insights

Rapamycin enhances non-small cell lung cancer (NSCLC) cell death under hypoxia by inhibiting survivin expression. This occurs via the hypoxia-inducible factor 1-alpha (HIF-1α) pathway, offering a potential therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Survivin, an apoptosis inhibitor, is overexpressed in tumors, including non-small cell lung cancer (NSCLC).
  • Understanding apoptosis regulation is crucial for developing targeted NSCLC therapies.

Purpose of the Study:

  • To investigate the effect of rapamycin on apoptosis and survivin expression in NSCLC cells under hypoxic conditions.
  • To elucidate the role of hypoxia-inducible factor 1-alpha (HIF-1α) in survivin regulation and rapamycin's mechanism of action.

Main Methods:

  • Utilized three human NSCLC cell lines (NCI-H1299, SK-MES-1, NCI-H460).
  • Analyzed apoptosis, survivin mRNA/protein expression under normoxia/hypoxia with/without rapamycin.
  • Employed siRNA and ChIP assays to assess HIF-1α's role in survivin regulation.

Main Results:

  • Rapamycin significantly increased NSCLC cell apoptosis under hypoxia.
  • Rapamycin inhibited hypoxia-induced survivin expression in NSCLC cell lines.
  • HIF-1α participates in hypoxia-induced survivin expression; rapamycin enhances HIF-1α degradation, inhibiting its expression.

Conclusions:

  • Rapamycin induces NSCLC apoptosis by inhibiting HIF-1α-mediated survivin expression under hypoxia.
  • This study reveals a novel therapeutic mechanism for rapamycin in NSCLC treatment.

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