2. Academic Validation
  3. Taxifolin regulates SLC31A1-mediated cuproptosis and tumor progression in hepatocellular carcinoma

Taxifolin regulates SLC31A1-mediated cuproptosis and tumor progression in hepatocellular carcinoma

  • Hum Cell. 2025 Jan 3;38(2):37. doi: 10.1007/s13577-024-01168-6.
Jike Li 1,  Yuelian Wang 2,  Lei Bao 3,  Guo Chen 4,  Qing Ye 5,  Chengshi He 6,  Lin Liu 7,  Mei Luo 8
Affiliations

Affiliations

  • 1 Traditional Chinese Medicine Laboratory, Chengdu Public Health Clinical Center, Chengdu, 610061, People's Republic of China.
  • 2 Center for Precision and Translational Medicine, Chengdu Public Health Clinical Center, Chengdu, 610061, People's Republic of China.
  • 3 Department of Internal Medicine, Chengdu Public Health Clinical Center, Chengdu, 610061, People's Republic of China.
  • 4 Department of Infectious Diseases, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, People's Republic of China.
  • 5 Department of Integrated Traditional & Western Medicine, Chengdu Public Health Clinical Center, Chengdu, 610061, People's Republic of China.
  • 6 Respiratory Medicine, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, People's Republic of China.
  • 7 Department of Nephrology, Panzhihua Central Hospital, Panzhihua, 617067, Sichuan, People's Republic of China.
  • 8 Infectious Disease Laboratory, Chengdu Public Health Clinical Center, Chengdu, 610061, People's Republic of China. phccidl_lm@163.com.
PMID: 39752031 DOI: 10.1007/s13577-024-01168-6
Abstract

Hepatocellular carcinoma (HCC) is a primary malignant neoplasm exhibiting a high mortality rate. Taxifolin is a naturally occurring flavonoid compound that exhibits a range of pharmacological properties. The effects of taxifolin on HCC remain largely unexplored. Therefore, the aim of this study was to examine the potential roles of taxifolin in the development and progression of HCC. In this study, CCK-8 assay was utilized to examine the impact of taxifolin on the cell viability. The copper ions level and the activity of mitochondrial respiratory chain were determined by the correspondent kits. The biological properties of HCC cells were evaluated using colony formation, transwell, flow cytometry, and TUNEL assays, respectively. Transcriptome Sequencing was carried out either with or without taxifolin treatment. The expression of cuproptosis-related proteins was determined by Western blot. We observed significant decrease of cell viability, Glutathione (GSH), and mitochondrial respiratory chain under the treatment of taxifolin, while an increase of copper ions level. Taxifolin was observed to suppress HCC progression both in vitro and in vivo. The intersection analysis was performed between upregulated genes and cuproptosis-related genes to obtain one intersection gene-SLC31A1. The knockdown of SLC31A1 reversed the tumor-suppressive effects induced by taxifolin. Taxifolin inhibited HCC progression through inducing Cuproptosis in an SLC31A1-mediated manner.

Keywords

Copper; Cuproptosis; Hepatocellular carcinoma; SLC31A1; Taxifolin.

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