BACKGROUND: The c-Jun N-terminal kinase (JNK) is thought to be involved in 
inflammation, proliferation and apoptosis.
AIM: To examine the role of JNK isoforms in metastasis, proliferation, migration 
and invasion of the malignant melanoma (MM) cell lines SK-MEL-28, SK-MEL-3 and 
WM164, using a kinase-specific inhibitor or isoform-specific small interfering 
(si)RNAs.
RESULTS: SK-MEL-3, a cell line established from metastatic MM, showed slightly 
increased phosphorylation of both JNK1 and JNK2, whereas WM164, a cell line 
derived from primary MM, showed significant phosphorylation of JNK1. A JNK 
inhibitor, SP600125, inhibited cell proliferation of SK-MEL-3 but not SK-MEL-28 
or WM164. Transfection of JNK1-specific siRNA reduced the migratory activity of 
WM164 cells, while silencing of either JNK1 or JNK2 strongly suppressed the 
invasive activity of SK-MEL-3.
CONCLUSIONS: Our study suggests that JNK isoforms have different roles in MM. 
Metastasis of MM may be regulated by JNK2, while invasion is regulated by both 
JNK1 and JNK2. JNK1 and JNK2 respectively mediate cell migration and cell 
proliferation. Further understanding of the specific roles of JNK isoforms in 
the pathogenesis of MM may lead to the development of therapies targeting 
specific isoforms.