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Rapamycin suppresses ROS-dependent apoptosis caused by selenomethionine in A549 lung carcinoma cells

Maiko Suzuki1, Manabu Endo, Fumiaki Shinohara

  • 1Department of Microbiology and Immunology, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan.

Cancer Chemotherapy and Pharmacology
|August 4, 2010
PubMed
Abstract

Insights

Selenium compounds like seleno-L-methionine (SeMet) induce apoptosis in cancer cells. Rapamycin suppresses SeMet-induced apoptosis via the Akt/mTOR/ROS pathway in lung cancer cells.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Selenium compounds exhibit chemotherapeutic properties by inducing apoptosis in cancer cells with minimal toxicity to normal cells.
  • The precise mechanisms of selenium's anti-cancer activity, particularly concerning apoptosis induction, require further elucidation.
  • Investigating the role of specific selenium compounds and their interaction with cellular pathways is crucial for understanding their therapeutic potential.

Purpose of the Study:

  • To investigate the effects of rapamycin on apoptosis induced by seleno-L-methionine (SeMet) and selenite in A549 lung adenocarcinoma cells.
  • To explore the signaling pathways involved in SeMet- and selenite-induced apoptosis.
  • To determine the role of the Akt/mTOR pathway in SeMet-induced apoptosis.

Main Methods:

  • Human adenocarcinoma A549 cells were treated with SeMet or selenite.
  • Cell proliferation and apoptosis were assessed using flow cytometry (TUNEL method).
  • Signaling molecules were analyzed via immunoblotting, with a focus on the Akt/mTOR pathway and reactive oxygen species (ROS) generation.

Main Results:

  • SeMet induced apoptosis in A549 cells, accompanied by reactive oxygen species (ROS) generation, which was blocked by N-acetyl-L-cysteine.
  • Rapamycin completely inhibited apoptosis induced by SeMet, but not by selenite.
  • SeMet-induced apoptosis was significantly downregulated by PI3K inhibitors, and rapamycin pretreatment inhibited ROS generation, suggesting involvement of the Akt/mTOR pathway.

Conclusions:

  • SeMet-induced apoptosis in A549 lung cancer cells is mediated by the Akt/mTOR/ROS pathway.
  • Akt appears to play an anti-survival role in SeMet-treated lung cancer cells.
  • The precise role of autophagic signaling in this process remains to be fully determined.

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