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Anti‐proliferative effect of ethylacetate fraction from Orostachys japonicus on modulation of MAPK signaling pathways in human gastric cancer cells
Author(s) -
Ryu DeokSeon,
Kim SeonHee,
Kwon JiHye,
Lee DongSeok
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.727.9
Subject(s) - mapk/erk pathway , p38 mitogen activated protein kinases , cell cycle , propidium iodide , signal transduction , kinase , chemistry , protein kinase a , cyclin dependent kinase 1 , microbiology and biotechnology , biology , cell , apoptosis , biochemistry , programmed cell death
This study focused on the anti‐proliferative effect of ethylacetate (EtOAc) fraction of the herbal plant Orostachys japonicus . This study examined the effect of EtOAc fraction on human gastric cancer (AGS) cell proliferation and investigated the underlying mitogen‐activated protein kinases (MAPK) signaling pathways. The EtOAc fraction inhibited the proliferation of AGS cells by inducing cell cycle arrest as evidenced by propidium iodide (PI) labeling and RT‐PCR analysis. In the cell cycle analyses, treatment with the EtOAc fraction resulted in a marked increase of cells in the sub‐G 1 and G 2 /M phases. RT‐PCR was performed to study the correlation between G 2 /M arrest and transcription of cell cycle control genes. The anti‐proliferative effect of EtOAc fraction was accompanied by inhibition of CDK1 and cyclin B1 mRNA. To understand the role of MAPK signaling in the anti‐proliferative effect of EtOAc fraction in AGS cells this study assessed EtOAc fraction‐treated AGS cells using antibodies against p38 MAPK (p38), c‐Jun N‐terminal kinase (JNK), and extracellular signal‐regulated kinase (ERK). MAPK such as p38, JNK, and ERK were analyzed by Western blotting. Treatment of AGS cells with the EtOAc fraction resulted in time‐ and dose‐dependent activation of p38, JNK, and ERK.