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Pterostilbene exerts antitumor activity via the Notch1 signaling pathway in human lung adenocarcinoma cells

Yang Yang1, Xiaolong Yan, Weixun Duan

  • 1Department of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an City, China.

Plos One
|May 15, 2013
PubMed

Insights

Pterostilbene (PTE) shows antitumor effects against lung cancer by increasing cell death and reactive oxygen species. Inhibiting Notch1 signaling enhances PTE

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Pterostilbene (PTE) exhibits potent antitumor properties, but its precise molecular mechanisms are not fully understood.
  • Lung adenocarcinoma is a significant global health concern, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To investigate the antitumor activity of PTE against human lung adenocarcinoma.
  • To elucidate the role of the Notch1 signaling pathway in PTE's anticancer effects.

Main Methods:

  • In vitro and in vivo studies using A549 lung adenocarcinoma cells.
  • Assessment of cell viability, mitochondrial membrane potential (MMP), glutathione levels, reactive oxygen species (ROS), and apoptosis.
  • Analysis of Notch1 Intracellular Domain (NICD) and Hes1 activation.
  • Utilized DAPT (gamma secretase inhibitor) and Notch1 siRNA to modulate Notch signaling.

Main Results:

  • PTE reduced lung adenocarcinoma cell viability in a dose- and time-dependent manner.
  • PTE induced apoptosis, increased ROS, decreased MMP, and reduced glutathione levels.
  • PTE activated Notch1 signaling (NICD and Hes1), which was inhibited by DAPT and Notch1 siRNA.
  • Notch1 inhibition sensitized cells to PTE and blocked pro-survival PI3K/Akt pathway activation.

Conclusions:

  • Lung adenocarcinoma cells activate Notch1 signaling as a survival response to PTE treatment.
  • Combining PTE with a gamma secretase inhibitor may offer a novel therapeutic strategy for lung adenocarcinoma by targeting cancer cell survival pathways.

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