ArticleDiscover oncology2025
Resveratrol synergizes with cisplatin to suppress osteosarcoma U2-OS cells via up-regulating Cx43 and inducing ROS-dependent apoptosis.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
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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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Who cites it
2 citing papers in PubMed.
- Correction: Resveratrol synergizes with cisplatin to suppress osteosarcoma U2-OS cells via up-regulating Cx43 and inducing ROS-dependent apoptosis.Discover oncology · 2026Article
- Resveratrol as a Modulator of Adriamycin-, Taxol-, and Cisplatin-Induced Cytotoxicity in MCF-7 Breast Cancer Cells.International journal of molecular sciences · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
backgroundResveratrol (Res), a plant-derived polyphenol, exerts synergistic effects when combined with various chemotherapeutic drugs, enhancing the antitumor activity of traditional chemotherapy. However, whether Res combined with cisplatin (CDDP) produces a synergistic inhibitory effect on osteosarcoma cell growth and its underlying mechanisms remain unclear.
methodsWe investigated the responses of U2-OS cells to Res, CDDP, or their combination using Cell Counting Kit-8 (CCK-8) for proliferation, flow cytometry for apoptosis, wound healing assays for migration, and Transwell assays for invasion. The effects of the two drugs on Wnt/β-catenin signaling were analyzed via quantitative real-time PCR (qRT-PCR) and western blotting. Additionally, the relationship between Cx43 and Wnt/Wnt/β-catenin signaling was explored by knocking down Cx43 using lentiviral infection.
resultsThe combination of Res and CDDP exhibited greater cytotoxicity against osteosarcoma U2-OS cells than either drug alone, and this effect was synergistic as determined by the Chou-Talalay equation. Cx43 knockdown attenuated the strong antitumor effect of the Res + CDDP combination and restored Wnt/β-catenin signaling activity. Furthermore, the Res + CDDP combination generated more reactive oxygen species (ROS) than individual treatments, inducing ROS-dependent apoptosis, which was blocked by N-acetylcysteine (NAC).
conclusionsRes combined with CDDP exerts a synergistic inhibitory effect on osteosarcoma by upregulating Cx43 and inducing ROS-dependent apoptosis. This study may provide a novel therapeutic strategy and potential clinical applications for osteosarcoma treatment.
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