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Pterostilbene exerts anticancer activity on non-small-cell lung cancer via activating endoplasmic reticulum stress
Zhiqiang Ma1, Yang Yang2,3,4, Shouyin Di1
1Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, 1 Xinsi Road, Xi'an, 710038, China.
Abstract:
Pterostilbene (PT), the natural dimethylated analog of resveratrol (RSV), is a potent anticarcinogen for non-small-cell lung cancer (NSCLC), but its anti-NSCLC mechanisms remain unclear. In this study, we show that PT treatment time- and dose-dependently enhanced the endoplasmic reticulum stress (ERS) signaling (i.e., p-PERK, IRE1, ATF4, CHOP), thus decreasing the cell viability and inducing apoptosis in human PC9 and A549 NSCLC cell lines. Moreover, the decreased migratory and adhesive abilities, downregulation of intracellular glutathione (GSH) level, enhanced reactive oxygen species (ROS) generation, Caspase 3 activity and mitochondrial membrane depolarization were observed in NSCLC cells treated with PT. These effects were reversed by CHOP siRNA which inhibited the ERS signaling pathway, but were promoted by thapsigargin (a classical ERS inducer) in vitro. Besides, in vivo studies also verify that PT exerted anticancer activity by mobilizing ERS signaling and apoptosis-related proteins, and these effects were enhanced by thapsigargin. Therefore, ERS activation may represent a new mechanism of anti-NSCLC action by PT, and a novel therapeutic intervention for lung cancer.
Insights
Pterostilbene (PT) enhances endoplasmic reticulum stress (ERS) signaling, reducing non-small-cell lung cancer (NSCLC) cell viability and inducing apoptosis. This suggests ERS activation is a novel therapeutic mechanism for PT against lung cancer.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Pterostilbene (PT), a resveratrol analog, shows anticarcinogenic potential against non-small-cell lung cancer (NSCLC).
- The precise molecular mechanisms underlying PT's anti-NSCLC effects are not fully understood.
Purpose of the Study:
- To investigate the anti-NSCLC mechanisms of Pterostilbene (PT).
- To determine if endoplasmic reticulum stress (ERS) signaling is involved in PT's anti-cancer activity.
Main Methods:
- Treatment of human PC9 and A549 NSCLC cell lines with PT.
- Analysis of ERS signaling pathway components (p-PERK, IRE1, ATF4, CHOP).
- Assessment of cell viability, apoptosis, migration, adhesion, glutathione (GSH) levels, reactive oxygen species (ROS) generation, Caspase 3 activity, and mitochondrial membrane potential.
- In vitro and in vivo studies using CHOP siRNA and thapsigargin.
Main Results:
- PT treatment dose- and time-dependently enhanced ERS signaling, decreasing cell viability and inducing apoptosis in NSCLC cells.
- PT reduced NSCLC cell migration and adhesion, downregulated GSH, increased ROS, and altered Caspase 3 activity and mitochondrial membrane potential.
- ERS inhibition via CHOP siRNA reversed PT's effects, while ERS induction with thapsigargin enhanced them.
- In vivo studies confirmed PT's anti-cancer activity via ERS and apoptosis modulation, enhanced by thapsigargin.
Conclusions:
- Endoplasmic reticulum stress (ERS) activation is a key mechanism for Pterostilbene's (PT) anti-NSCLC effects.
- PT's ability to induce ERS, apoptosis, and reduce cell viability offers a novel therapeutic strategy for lung cancer.
- Targeting ERS signaling presents a promising avenue for developing new lung cancer interventions.
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