Sulforaphane-cysteine elicits apoptosis through JNK-mediated caspase activation in oral squamous cell carcinoma cells.

Sulforaphane-cysteine (SFN-Cys) is a naturally-occurring form of plant-derived isothiocyanate metabolites that displays several tumor-suppressive properties. However, the oncostatic potential of SFN-Cys on oral squamous cell carcinoma (OSCC) is mostly elusive. In this study, we tried to test whether SFN-Cys affects OSCC to progress and further explored the underlying array of molecular cues that SFN-Cys mediates. Our results demonstrate that SFN-Cys was an effective inducer of cytotoxicity to OSCC cells, accompanied with blockage of cell cycling and promotion of apoptotic events. Moreover, treatment of OSCC cells with SFN-Cys attuned an apoptosis-associated protein regulatory program, underlined by downregulation of apoptosis suppressors (cIAP-1 and XIAP) and activation of caspase cascades. Furthermore, caspase activations in SFN-Cys-treated OSCC cells were affected by the pre-incubation with a specific c-Jun N-terminal kinase (JNK) inhibitor, suggesting a functional link of JNK pathway to SFN-Cys's actions in OSCC cells. Collectively, our data revealed that SFN-Cys hampered cell cycle progression and elicited apoptotic responses in OSCC via a JNK-mediated activation of caspase pathways. These findings provide possible avenues for the application of a natural compound in the management of oral malignancies.