N‑acetyl-S-(p-chlorophenylcarbamoyl)cysteine induces mitochondrial-mediated apoptosis and suppresses migration in melanoma cells

Oncology Reports
Wei ChenYutian Ling

Abstract

We previously reported that N-acetyl-S-(p-chlorophenylcarbamoyl)cysteine (NACC) induces apoptosis in human melanoma UACC-62 cells. In the present study, the molecular mechanism of NACC‑induced apoptosis in melanoma cells was investigated. Briefly, the apoptosis triggered by NACC was confirmed in UACC‑62 cells for shorter treatment periods. Increased activities of caspase‑3 and caspase‑9 but not caspase‑8 were observed in the cell lysates. Western blotting showed that the pro‑apoptotic protein Bax was upregulated and the anti‑apoptotic protein Mcl‑1 was downregulated and cytochrome c (Cyto c) was released into the cytosol. Flow cytometric analysis demonstrated that NACC induced significant mitochondrial membrane potential disruption. Significant increases in the generation of reactive oxygen species (ROS) and cytosolic calcium elevation were also observed. However, opening of the mitochondrial permeability transition pore which could be involved in Cyto c leakage from mitochondria was found to be unaffected by NACC. Taken together, all the results presented in this study including apoptotic induction, activation of the caspase‑3 and ‑9 cascade, upregulation of Bax, downregulation of Mcl‑1, Cyto c release from the mitochondria, m...Continue Reading

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