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Title 

Proteomic analysis and the antimetastatic effect of N-(4-methyl)phenyl-O-(4-methoxy) phenyl-thionocarbamate-induced apoptosis in human melanoma SK-MEL-28 cells

Authors 

S L ChoiY S ChoiY K KimN D SungChang-Won KhoByoung Chul ParkEun-Mi KimJeong-Hyung LeeK M KimM Y KimP K Myung

Publisher 

Pharmaceutical Society of Korea

Issue Date 

2006

Citation 

Archives of Pharmacal Research, vol. 29, no. 3, pp. 224-234

Keywords 

apoptosismetastasisN-(4-methyl)phenyl-O-(4-methoxy)phenyl- thionocarbamateproteome mapSK-MEL-26 cellsantineoplastic agentCASP4 protein, humancell cycle proteinCHES1 protein, humaninitiator caspase

Abstract 

We employed human SK-MEL-28 cells as a model system to identify cellular proteins that accompany N-(4-methyl)phenyl-O-(4-methoxy)phenyl-thionocarbamate (MMTC)-induced apoptosis based on a proteomic approach. Cell viability tests revealed that SK-MEL-28 skin cancer cells underwent more cell death than normal HaCaT cells in a dose-dependent manner after treatment with MMTC. Two-dimensional electrophoresis in conjunction with matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry analysis or computer matching with a protein database further revealed that the MMTC-induced apoptosis is accompanied by increased levels of caspase-1, checkpoint suppressor-1, caspase-4, NF-κB inhibitor, AP-2, c-Jun-N-terminal kinase, melanoma inhibitor, granzyme K, G1/S specific cyclin D3, cystein rich protein, Ras-related protein Rab-37 or Ras-related protein Rab-13, and reduced levels of EMS (oncogene), ATP synthase, tyrosine-phosphatase, Cdc25c, 14-3-3 protein or specific structure of nuclear receptor. The migration suppressing effect of MMTC on SK-MEL-28 cell was tested. MMTC suppressed the metastasis of SK-MEL-8 cells. It was also identified that MMTC had little angiogenic effect because it did not suppress the proliferation of HUVEC cell line. These results suggest that MMTC is a novel chemotherapeutic and metastatic agents against the SK-MEL-28 human melanoma cell line.

ISSN 

0253-6269

Link 

http://dx.doi.org/10.1007/BF02969398

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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