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Taraxasterol Suppresses Renal Cell Carcinoma Progression by Modulating Cell Cycle Progression and Apoptosis
Jiao-Gui Xie1, Xing-Chen Liu2, Xin-Wei Han3
1Clinical Laboratory Medicine, Tai Zhou Central Hospital (Taizhou University Hospital), Taizhou 318000, China.
Anti-Cancer Agents in Medicinal Chemistry
|March 15, 2026
Abstract
Introduction:
Renal cell carcinoma (RCC) is a common and aggressive urological malignancy with limited response to chemotherapy and radiotherapy. The search for effective, low-toxicity natural compounds is therefore of increasing interest. Taraxasterol (TAX), a pentacyclic triterpene from dandelion, has shown antitumor activity in several cancers, but its effects on RCC remain unexplored. To investigate the antitumor effects and underlying mechanisms of TAX on RCC in vitro and in vivo.
Methods: The human embryonic kidney cell HEK-293T and human RCC cells (786-O) were cultured and treated with different concentrations of TAX (0, 5, 10, and 15 µM), respectively. Next, the MTT assay was employed for detecting cell viability, the scratch assay for cell migration, the Transwell for cell invasion, flow cytometry for changes in mitochondrial membrane potential, apoptosis levels, and cell cycle, and the western blot for protein expression levels related to cell cycle and apoptosis. Additionally, a 786-O xenograft model was established in BALB/c nude mice to evaluate the in vivo antitumor effect of TAX. Tumor volume and weight were measured, and Ki-67 and cleaved Caspase-3 expression in tumor tissues were assessed via immunohistochemistry. Results: TAX did not affect the viability, apoptosis, or cell cycle of HEK-293T cells, but significantly inhibited proliferation, migration, and invasion of 786-O cells, while inducing apoptosis and G2/M arrest in a concentration-dependent manner. TAX reduced mitochondrial membrane potential, increased cleaved-Caspase-3 and cleaved-PARP, decreased Bcl-2, and downregulated Cyclin B1 and CDK1, while upregulating p21 and p27. In vivo, TAX suppressed tumor growth and reduced Ki-67, while increasing cleaved Caspase-3 expression in xenograft tumors. Discussion: These findings support TAX as a promising natural compound for RCC therapy. Further work is needed to validate its effects across additional RCC models and to explore other potential molecular pathways. Conclusion: TAX exerts antiproliferative, pro-apoptotic, and anti-invasive effects on RCC, highlighting its potential as a therapeutic candidate.Insights
Taraxasterol (TAX), a natural compound from dandelion, effectively inhibits renal cell carcinoma (RCC) growth, migration, and invasion by inducing apoptosis. This study highlights TAX as a potential therapeutic agent for RCC, demonstrating significant antitumor effects in vitro and in vivo.
Area of Science:
- Pharmacology
- Oncology
- Natural Products Chemistry
Background:
- Renal cell carcinoma (RCC) is an aggressive cancer with limited treatment options.
- Natural compounds are being explored for their therapeutic potential in cancer treatment.
- Taraxasterol (TAX), a triterpene from dandelion, has shown antitumor activity but its role in RCC was unknown.
Purpose of the Study:
- To investigate the antitumor effects of Taraxasterol (TAX) on renal cell carcinoma (RCC) cells.
- To elucidate the underlying molecular mechanisms of TAX's action in RCC.
- To evaluate the efficacy of TAX in a preclinical in vivo model of RCC.
Main Methods:
- In vitro studies utilized MTT assay, scratch, Transwell assays, flow cytometry, and Western blotting on RCC cells.
- In vivo efficacy was assessed using a 786-O xenograft mouse model.
- Analysis included cell viability, proliferation, migration, invasion, apoptosis, cell cycle, mitochondrial membrane potential, and protein expression.
Main Results:
- TAX demonstrated significant antiproliferative, anti-migratory, and anti-invasive effects on 786-O RCC cells without affecting normal kidney cells.
- TAX induced apoptosis and G2/M cell cycle arrest, reduced mitochondrial membrane potential, and modulated key proteins involved in apoptosis and cell cycle regulation.
- In vivo, TAX suppressed tumor growth, reduced proliferation marker Ki-67, and increased apoptosis marker cleaved Caspase-3 in xenograft tumors.
Conclusions:
- Taraxasterol (TAX) exhibits potent antiproliferative, pro-apoptotic, and anti-invasive properties against renal cell carcinoma (RCC).
- TAX demonstrates significant potential as a therapeutic candidate for RCC treatment.
- Further research is warranted to explore TAX's efficacy in diverse RCC models and its broader molecular pathways.
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