ArticleAntioxidants (Basel, Switzerland)2021
Shikonin Induced Program Cell Death through Generation of Reactive Oxygen Species in Renal Cancer Cells.
Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Research progress in metabolic reprogramming and targeting metabolic pathways for clear cell renal cell carcinoma.Genes & diseases · 2026Review
- Systematic characterization of the R2R3-MYB family in Lithospermum erythrorhizon and regulatory mechanisms of LeMYB1 in shikonin biosynthesis.BMC plant biology · 2026Article
- Single-cell sequencing-guided design of synergistic chemo-immunotherapy nanodrugs for cGAS-STING activation in prostate cancer therapy.Journal of nanobiotechnology · 2026Article
- Shikonin as a Dietary Phytochemical with Multi-Target Anti-Cancer Activities: From Molecular Mechanisms to Translational Applications.Nutrients · 2025Review
- Natural products for enhancing the sensitivity or decreasing the adverse effects of anticancer drugs through regulating the redox balance.Chinese medicine · 2024Review
- GHITM regulates malignant phenotype and sensitivity to PD-1 blockade of renal cancer cells via Notch signalling.Journal of cellular and molecular medicine · 2024Article
- Research progress in mechanism of anticancer action of shikonin targeting reactive oxygen species.Frontiers in pharmacology · 2024Review
- Novel Strategies for Tumor Treatment: Harnessing ROS-Inducing Active Ingredients from Traditional Chinese Medicine Through Multifunctional Nanoformulations.International journal of nanomedicine · 2024Review
- Shikonin Induces Autophagy and Apoptosis in Esophageal Cancer EC9706 Cells by Regulating the AMPK/mTOR/ULK Axis.Analytical cellular pathology (Amsterdam) · 2024Article
- Patient-derived tumor models: a suitable tool for preclinical studies on esophageal cancer.Cancer gene therapy · 2023Review
- Shikonin promotes rat periodontal bone defect repair and osteogenic differentiation of BMSCs by p38 MAPK pathway.Odontology · 2023Article
- Identification of a novel combination treatment strategy in clear cell renal cell carcinoma stem cells with shikonin and ipilimumab.Frontiers in immunology · 2023Article
- Roles of DNA damage repair and precise targeted therapy in renal cancer (Review).Oncology reports · 2022Article
- Article
- Exosomes: A novel insight into traditional Chinese medicine.Frontiers in pharmacology · 2022Review
- Ononin Shows Anticancer Activity Against Laryngeal CancerFrontiers in oncology · 2022Article
- Shikonin induces ferroptosis in multiple myelomaFrontiers in oncology · 2022Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Shikonin mitigated tumor cell proliferation by elevating reactive oxygen species (ROS) levels. Herein, we investigated the effects of shikonin on renal cancer cell (RCC) cell proliferation. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay indicated that shikonin dose-dependently reduced the proliferation of Caki-1 and ACHN cells. Shikonin remarkably triggered necrosis and apoptosis in Caki-1 and ACHN cells in proportion to its concentration. Moreover, necrostatin-1 recovered cell viability in the presence of shikonin. Elevated ROS levels and mitochondrial dysfunction were also found in shikonin treatment groups. Pretreatment with N-acetyl cysteine remarkably mitigated shikonin-induced cell death and ROS generation. Western blot analysis revealed that shikonin reduced pro-PARP, pro-caspase-3, and Bcl-2 expression and increased cleavage PARP expression. Enhanced autophagy was also found in the shikonin-treated group as evidenced by acridine orange staining. Moreover, light chain 3B (LC3B)-II accumulation and enhanced p62 expression indicated that autophagy occurred in the shikonin-treated group. LC3B knockdown considerably recovered cell viability in the presence of shikonin. Shikonin treatment elevated p38 activity in a dose-dependent manner. In conclusion, our results revealed that shikonin triggered programmed cell death via the elevation of ROS level and p38 activity in different types of RCC cells. These findings suggested that shikonin may be a potential anti-RCC agent.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.