Mechanism of Cryptotanshinone Targeting HK2 to Induce Apoptosis in Mouse Hepatoma H22 Cells

Authors

  • Peiling Xu School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 310053 Hangzhou, Zhejiang, China Author
  • Hanlei Huang School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 310053 Hangzhou, Zhejiang, China Author
  • Huijun Zeng School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 310053 Hangzhou, Zhejiang, China Author
  • Zhaohuan Lou School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 310053 Hangzhou, Zhejiang, China Author
  • Lifeng Lifeng Department of Surgical Oncology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, 310052 Hangzhou, Zhejiang, China Author
  • Zeying Liu School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 310053 Hangzhou, Zhejiang, China Author

DOI:

https://doi.org/10.62767/

Keywords:

cryptotanshinone, HK2, hepatocarcinoma, mouse hepatoma H22 cell, glycolysis

Abstract

Objective: To observe the anti-liver cancer effect of cryptotanshinone (CTS) in vitro, and to explore the mechanism of targeting hexokinase 2 (HK2) to regulate glycolytic pathway and induce apoptosis in hepatoma carcinoma cells. Methods: In in vitro cell experiments, CCK-8 method was used to detect the effects of different concentrations (1, 2, 5, 10, 20, 40, 80, 100, 200 μmol/L) of CTS on the viability of H22 cells at different time periods (24 h/48 h). The effects of different concentrations (5, 10, 20 μmol/L) of CTS on glucose uptake, lactate production, apoptosis, and the expressions of HK2, Bcl-2 and Cyt-c proteins in H22 cells were detected using GOD-POD method, lactate oxidase method, Annexin V-FITC/PI double staining method and Western blot, respectively, after 48 h of intervention. Results: CTS significantly inhibited the proliferation of H22 cells in a concentration- and time-dependent manner, with a 48-hour half-inhibitory concentration (IC50) of 24.43 μmol/L. CTS suppressed glucose uptake and lactate production in H22 cells, suggesting that it attenuated the energy metabolism of tumor cells by inhibiting the glycolytic pathway. CTS down-regulated the expressions of HK2 and Bcl-2 proteins, and up-regulated the expression of Cyt-c protein, implying that CTS induced apoptosis in hepatoma cells by repressing the HK2-mediated glycolysis pathway and regulating the mitochondrial apoptosis pathway. Conclusion: CTS evidently induces apoptosis in H22 cells by inhibiting the HK2-mediated glycolysis pathway and regulating the mitochondrial apoptosis pathway, which has potential anti-liver cancer effects

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Published

2026-09-30

Data Availability Statement

The data presented in this study are available on request from the corresponding author.

Issue

Section

Original Research

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