In recent years, an increase in melanoma incidence associated with rapidly growing mortality rate has been observed. The prevalence of disease doubles almost every 10 years and grows much faster than in other malignant tumors [1]. Over the years, many risk factors for melanoma, both exogenous (eg. UV radiation) and endogenous (genetic predispositions), have been identified. However, unraveling the etiology of this disease requires further investigation.Melanoma aggressiveness is related to the ability to rapid metastasis, high proliferative activity of cells, wide range of genetic and epigenetic changes and high resistance to conventional treatment [2]. Due to these reasons, there is a great demand for new anti-melanoma therapies.

Currently, it is considered that valproic acid (VPA) may be an effective agent in the therapy of malignant melanoma. The VPA is the histone deacetylase inhibitor (HDACi), and is involved in maintaining a balance between the acetylation and deacetylation of histones [3].

The aim of the study was to evaluate the effect of VPA on proliferation and apoptosis in human melanoma cells.

The study material was human melanoma cell line (G-361). The influence of VPA on cell growth rate was tested using XTT assay (Sigma-Aldrich®). The ability of VPA to induce apoptosis was determined by measuring the activity of caspase-3 using “Caspase-3 Assay Kit, Colorimetric” (Sigma-Aldrich®).

It was found that higher concentrations (1, 3, 5, 10 mM) of VPA inhibited proliferation of melanoma cells. The lowest concentration (0.3 mM) of VPA was insufficient to reduce the proliferative activity of the G-361 cells. To determine the apoptotic effect of VPA in the melanoma cells, caspase-3 activity was measured after 48-hr exposure to VPA at concentrations of 1, 5 and 10 mM. The statistically significant increase in caspase-3 activity in treated cells (5 and 10 mM VPA) compared to control was observed.

References

1. Völler D, Ott C, Bosserhoff A. MicroRNAs in malignant melanoma. Clin Biochem 2013; doi: 10.1016/j.clinbiochem.2013.01.008.
2. Chodurek E, Gołąbek K, Orchel J, Orchel A, Dzierżewicz Z. Znaczenie epigenetyki w patogenezie czerniaka. Ann Acad Med Siles 2012; 66 (3): 44–56.
3. Grabarska A, Dmoszyńska-Graniczka M, Nowosadzka E, Stepulak A. Histone deacetylase inhibitors - molecular mechanisms of actions and clinical applications. Postepy Hig Med Dosw 2013; 67:722-35.

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