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Inhibition of Liver Cancer Cell Viability by Triazole through Up-regulation of p38 Phosphorylation and Targeting the Activation of p-ERK1/2 and Akt Protein Expression

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Abstract

The present study was aimed to explore the effect of triazole on growth and viability of liver cancer cells. Cell growth was examined using the MTT test and expression of several proteins was assessed by western blotting assay. The Matrigel-coated Transwell assay was employed to examine the infiltration of cells. The data from MTT assay showed that MHCC97H and H4TG liver cancer cell viability was inhibited by triazole in a concentration-dependent manner. After treatment with 0.5, 1.0, 2.0, 4, 8, and 16 µM doses of triazole, the rate of H4TG cell viability was decreased to 96, 73, 58, 39, 29, and 28%, respectively. Treatment of MHCC97H cells with 0.5, 1.0, 2.0, 4, 8, and 16 µM doses of triazole resulted in a reduction in cell viability to 94, 70, 53, 35, 22, and 21%, respectively. Triazole treatment also led to a significant reduction in MHCC97H cell invasiveness compared to the control cells. In MHCC97H cells treated with triazole, there was a noticeable decrease in the levels of p-ERK1/2, and p-Akt protein expression. Treatment of MHCC97H cells with triazole resulted in a prominent increase in p-p38 level. In summary, triazole inhibits growth and viability of liver cancer cells through targeting the activation of p-ERK1/2 and Akt proteins. Therefore, triazole may be investigated further as a therapeutic agent for the treatment of liver cancer.

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This work was supported by ongoing institutional funding. No additional grants to carry out or direct this particular research were obtained.

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Authors and Affiliations

  1. Interventional Vascular Surgery, Affiliated Hospital of Hebei University, 071000, Baoding, Hebei Province, China

    Shanfeng Li, Long Zhou, Feng Zhao, Haisong Wang & Meng Sun

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  1. Shanfeng Li
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  2. Long Zhou
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Correspondence to Meng Sun.

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ETHICS APPROVAL AND CONSENT TO PARTICIPATE

This work does not contain any studies involving human and animal subjects. Data analysis was performed from the open-access database Pulse Transit Time PPG Dataset (version 1.1.0) [9]. According to the Pulse Transit Time PPG Dataset data, all studies were conducted in accordance with the principles of biomedical ethics set out in the 1964 Declaration of Helsinki and its subsequent amendments, and all participants provided written informed consent.

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Shanfeng Li, Zhou, L., Zhao, F. et al. Inhibition of Liver Cancer Cell Viability by Triazole through Up-regulation of p38 Phosphorylation and Targeting the Activation of p-ERK1/2 and Akt Protein Expression. Dokl Biochem Biophys (2024). https://doi.org/10.1134/S1607672923600525

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