ArticleOncology letters2020
Autophagy suppresses resveratrol-induced apoptosis in renal cell carcinoma 786-O cells.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- ORM1 Mediates Ln-IgG-Induced Podocyte Damage and Autophagy via the AMPK/mTOR Signaling.Organogenesis · 2025Article
- Natural anti-cancer products: insights from herbal medicine.Chinese medicine · 2025Review
- The Interplay Between Autophagy and Apoptosis in the Mechanisms of Action of Stilbenes in Cancer Cells.Antioxidants (Basel, Switzerland) · 2025Review
- Metformin combined with rapamycin ameliorates podocyte injury in idiopathic membranous nephropathy through the AMPK/mTOR signaling pathway.Journal of cell communication and signaling · 2023Article
- Polyphenols and Their Metabolites in Renal Diseases: An Overview.Foods (Basel, Switzerland) · 2022Review
- Progress in Natural Compounds/siRNA Co-delivery Employing Nanovehicles for Cancer Therapy.ACS combinatorial science · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a polyphenolic compound, resveratrol (Res) is widely distributed in a variety of plants. Previous studies have demonstrated that Res can inhibit various different types of tumor growth. However, its role in renal cell carcinoma (RCC) remains largely unknown. The present study first demonstrated that Res inhibited cell viability and induced apoptosis in RCC 786-O cells. Further experiments revealed that Res damaged the mitochondria and activated caspase 3. In contrast, Z-VAD-FMK, a pan-caspase inhibitor, suppressed Res-induced apoptosis. Reactive oxygen species (ROS) were involved in the process of Res-induced apoptosis, and antioxidant N-acetyl cysteine could significantly attenuate this. Furthermore, Res activated c-Jun N-terminal kinase via ROS to induce autophagy, whereas inhibition of autophagy with chloroquine or Beclin 1 small interfering RNA aggravated Res-induced apoptosis, indicating that autophagy served as a pro-survival mechanism to protect 786-O cells from Res-induced apoptosis. Therefore, a combination of Res and autophagy inhibitors could enhance the inhibitory effect of Res on RCC.
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Registered trials
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