ArticleScientific reports2017
Pterostilbene exerts anticancer activity on non-small-cell lung cancer via activating endoplasmic reticulum stress.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Functional roles and clinical implications of pseudogenes signatures as emerging biomarkers in cancer.Discover oncology · 2026Review
- Pterostilbene in the Management and Treatment of Multiple Myeloma.Current issues in molecular biology · 2026Review
- Pterostilbene in Oxidative Stress-Related Diseases: Context-Dependent Regulation of Redox Homeostasis and Translational Challenges.Drug design, development and therapy · 2026Review
- Nutraceuticals for Preventing and Managing Cancer Chemotherapy-Induced Cardiotoxicity: An Updated Comprehensive Review.Cardiology research and practice · 2026Review
- Inflammation in cardiovascular-kidney-metabolic syndrome: key roles and underlying mechanisms-a comprehensive review.Molecular and cellular biochemistry · 2025Review
- Polydatin: A natural compound with multifaceted anticancer properties.Journal of traditional and complementary medicine · 2025Review
- Pterostilbene as a Multifaceted Anticancer Agent: Molecular Mechanisms, Therapeutic Potential and Future Directions.Medical oncology (Northwood, London, England) · 2025Review
- TROP2 regulates cisplatin sensitivity of triple-negative breast cancer cells by regulating endoplasmic reticulum stress.Histology and histopathology · 2025Article
- Advances in antitumor effects of pterostilbene and its derivatives.Future medicinal chemistry · 2025Review
- Endoplasmic reticulum stress in non-small cell lung cancer: a review of therapeutic agents, mechanistic insights, and implications for therapy.Frontiers in cell and developmental biology · 2025Review
- TROP2 promotes the proliferation of triple-negative breast cancer cells via calcium ion-dependent ER stress signaling pathway.Cell biochemistry and biophysics · 2024Article
- Pterostilbene-Mediated Inhibition of Cell Proliferation and Cell Death Induction in Amelanotic and Melanotic Melanoma.International journal of molecular sciences · 2023Article
- Pterostilbene in the treatment of inflammatory and oncological diseases.Frontiers in pharmacology · 2023Review
- Uncovering the Anticancer Potential of Polydatin: A Mechanistic Insight.Molecules (Basel, Switzerland) · 2022Review
- Role of Plant-Derived Active Constituents in Cancer Treatment and Their Mechanisms of Action.Cells · 2022Review
- Mechanism of Pterostilbene-Induced Cell Death in HT-29 Colon Cancer Cells.Molecules (Basel, Switzerland) · 2022Article
- The role of XBP-1-mediated unfolded protein response in colorectal cancer progression-a regulatory mechanism associated with lncRNA-miRNA-mRNA network.Cancer cell international · 2021Article
- Pterostilbene promotes mitochondrial apoptosis and inhibits proliferation in glioma cells.Scientific reports · 2021Article
- Toxicological Evaluation of Piceatannol, Pterostilbene, and ε-Viniferin for Their Potential Use in the Food Industry: A Review.Foods (Basel, Switzerland) · 2021Review
- High expression of PIG11 correlates with poor prognosis in gastric cancer.Experimental and therapeutic medicine · 2021Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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