ReferenceID 5506
Shikonin Induced Program Cell Death through Generation of Reactive Oxygen Species in Renal Cancer Cells
Antioxidants (Basel)
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
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Record Fields
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- Reference Id
- 5506
- Evidence Id
- 22096
- Core Evidence Id
- 22096
- Source Reference Id
- 4255
- Herb2 Reference Id
- HBREF005052
- Subject Paper Key
- HBIN030442_34829701
- Pubmed Id
- 34829701
- Doi
- 10.3390/antiox10111831
- Paper Title
- Shikonin Induced Program Cell Death through Generation of Reactive Oxygen Species in Renal Cancer Cells
- Paper 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.
- Journal
- Antioxidants (Basel)
- Publish Year
- 2021
- Experiment Subject
- Experiment Type
- Cell Experiment
- Phenotype Related
- Mitochondrial Dysfunction; Tumor; Renal Cancer
- Paper Title Cn
- Paper Title En
- Shikonin Induced Program Cell Death through Generation of Reactive Oxygen Species in Renal Cancer Cells
- Bilingual Status
- semi_complete