ArticleIranian journal of pharmaceutical research : IJPR
Traditional Chinese Medicine Approach to Renal Cell Carcinoma: Jing-Si Herbal Tea Triggers Apoptosis and Ferroptosis in HK-2 Cells.
Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Jing-Si Herbal Tea as a multitargeted complementary therapy: Evidence from preclinical and clinical studies.Tzu chi medical journalReview
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5 authors.
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Abstract
Background: Renal cell carcinoma (RCC) is the most common malignant tumor of the kidney, with clear cell renal cell carcinoma (ccRCC) representing its predominant subtype. Despite significant advances in targeted and immune therapies, treatment resistance and recurrence continue to pose major challenges, underscoring the urgent need for novel therapeutic strategies. Jing-Si Herbal Tea (JSHT), a traditional Chinese medicine (TCM) formulation, has demonstrated anti-tumor, anti-inflammatory, and antioxidant properties; however, its mechanisms of action in kidney disease and cancer remain poorly understood. Methods: Human proximal tubule epithelial (HK-2) cells were treated with various concentrations of JSHT (0%, 4%, and 8%) for 24 and 48 hours. Cell viability was assessed using the WST-1 assay. The expression levels of cleaved-caspase 3, glutathione peroxidase 4 (GPX4), and solute carrier family 7 member 11 (SLC7A11) were analyzed by western blotting and quantified relative to β-actin. Results: The JSHT significantly reduced HK-2 cell viability in a time- and concentration-dependent manner. Treatment with JSHT resulted in upregulation of cleaved-caspase 3, indicating activation of apoptosis, while concurrently downregulating GPX4 and SLC7A11, which are key regulators of ferroptosis resistance. These findings demonstrate that JSHT induces two forms of regulated cell death - ferroptosis and apoptosis - in renal epithelial cells. Conclusions: The JSHT exhibits antiproliferative effects in HK-2 cells by promoting apoptosis and sensitizing cells to ferroptosis through suppression of GPX4 and SLC7A11. These results provide preliminary mechanistic insights into the effects of JSHT and indicate its potential relevance for future research in RCC. However, validation in RCC-specific models and in vivo systems is necessary. A notable limitation of this study is the use of a non-cancerous renal cell line; thus, the in vitro findings may not fully recapitulate tumor biology. Future studies employing RCC cell lines, patient-derived tumor models, and in vivo validation are warranted to elucidate the therapeutic potential of JSHT as a complementary approach for RCC management.
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