The Journal of Practical Medicine ›› 2025, Vol. 41 ›› Issue (6): 781-789.doi: 10.3969/j.issn.1006-5725.2025.06.002

• Basic Research • Previous Articles    

The effect of vanadyl bis(acetylacetonato) on the proliferation and invasion of human adrenocortical carcinoma cells

Meiyu GAN,Chunjiao WU,Jingyi QIN,Zuojie. LUO()   

  1. Department of Endocrinology,the First Affiliated Hospital of Guangxi Medical University,Nanning 530021,Guangxi,China
  • Received:2024-12-24 Online:2025-03-25 Published:2025-03-31
  • Contact: Zuojie. LUO E-mail:luozuojie@gxmu.edu.cn

Abstract:

Objective To investigate the effects of bis(acetylacetonato)oxovanadium(IV) [VO(acac)?] on human adrenocortical carcinoma cell lines SW?13 and NCI?H295R in vitro, aiming to determine whether VO(acac)? promotes or inhibits the proliferation, migration, and invasion of these cells. Methods SW?13 and NCI?H295R cells in logarithmic growth phase were exposed to VO(acac)? at concentrations of 6.25, 12.5, 25, 50, 75, 100, and 200 μmol/L for 24 and 48 hours, respectively. Mitotane served as the positive control. Cell viability was assessed using the CCK?8 assay to evaluate the effects of VO(acac)? on SW?13 and NCI?H295R cells. Subsequently, cells were treated with VO(acac)? at concentrations of 0, 6.25, 12.5, and 25 μmol/L for 48 hours, and flow cytometry was employed to investigate the impact of VO(acac)? on apoptosis. The migratory ability of the cells was evaluated using a wound healing assay, while their invasive capacity was assessed via a Transwell assay. Additionally, the clonogenic assay was used to determine the proliferative potential of SW?13 and NCI?H295R cells following VO(acac)? treatment. Results The CCK?8 results demonstrated that VO(acac)2 inhibited the viability of SW?13 and NCI?H295R cells in a time? and concentration?dependent manner. Specifically, the half?maximal inhibitory concentrations (IC50) for VO(acac)2 against SW?13 cells were 62.98 ± 6.67 μmol/L after 24 hours and (14.61 ± 1.66) μmol/L after 48 hours of treatment, while the corresponding IC50 values for NCI?H295R cells were 46.78 ± 7.89 μmol/L and 12.61 ± 2.98 μmol/L, respectively. Flow cytometry analysis revealed that VO(acac)2 induced apoptosis in both SW?13 and NCI?H295R cells in a concentration?dependent manner (P < 0.05). The wound healing assay indicated a significant reduction in the migratory rate of SW?13 and NCI?H295R cells with increasing concentrations of VO(acac)2P < 0.05). Transwell assay results showed that VO(acac)2 significantly inhibited the invasive ability of SW?13 and NCI?H295R cells in a concentration?dependent fashion. Finally, the clonogenic assay confirmed that VO(acac)2 suppressed the proliferative capacity of SW?13 and NCI?H295R cells in a concentration?dependent manner. Conclusion VO(acac)2 inhibits the proliferation, migration, and invasion of human adrenocortical carcinoma cells (SW?13 and NCI?H295R), while inducing apoptosis in these cell lines.

Key words: vanadyl bis(acetylacetonato), adrenocortical carcinoma, proliferation, invasion, apoptosis

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