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Role of c‐ J un N ‐terminal kinase isoforms in the cellular activity of melanoma cell lines
Author(s) -
KogushiNishi H.,
Jinnin M.,
Kobayashi Y.,
Muchemwa F. C.,
Hirano A.,
Makino T.,
Fukushima S.,
Masuguchi S.,
Ishihara T.,
Inoue Y.,
Ihn H.
Publication year - 2013
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/ced.12102
Subject(s) - kinase , gene isoform , cell growth , cell culture , phosphorylation , gene silencing , cancer research , transfection , microbiology and biotechnology , c jun , apoptosis , cell , biology , biochemistry , gene , transcription factor , genetics
Summary Background The c‐ J un 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 WM 164, using a kinase‐specific inhibitor or isoform‐specific small interfering (si) RNA s. Results SK ‐ MEL ‐3, a cell line established from metastatic MM , showed slightly increased phosphorylation of both JNK 1 and JNK 2, whereas WM 164, a cell line derived from primary MM , showed significant phosphorylation of JNK 1. A JNK inhibitor, SP 600125, inhibited cell proliferation of SK ‐ MEL ‐3 but not SK ‐ MEL ‐28 or WM 164. Transfection of JNK 1‐specific si RNA reduced the migratory activity of WM 164 cells, while silencing of either JNK 1 or JNK 2 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 JNK 2, while invasion is regulated by both JNK 1 and JNK 2. JNK 1 and JNK 2 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.