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Apoptosis signal‐regulating kinase‐1 inhibitor as a potent therapeutic drug for the treatment of gastric cancer
Author(s) -
Hayakawa Yoku,
Hirata Yoshihiro,
Sakitani Kosuke,
Nakagawa Hayato,
Nakata Wachiko,
Kinoshita Hiroto,
Takahashi Ryota,
Takeda Kohsuke,
Ichijo Hidenori,
Maeda Shin,
Koike Kazuhiko
Publication year - 2012
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12024
Subject(s) - ask1 , cell growth , apoptosis , cancer research , trastuzumab , kinase , cancer , downregulation and upregulation , in vivo , growth inhibition , cancer cell , signal transduction , biology , pharmacology , protein kinase a , microbiology and biotechnology , cyclin dependent kinase 2 , biochemistry , genetics , breast cancer , gene
Aside from the human epidermal growth factor receptor‐2 ( HER 2)‐targeting agent trastuzumab, molecular targeting therapy for gastric cancer ( GC ) has not been established. We previously reported that apoptosis signal‐regulating kinase‐1 ( ASK 1) was upregulated in human GC and that overexpression of ASK 1 promoted GC cell proliferation. Here, we investigated the effect of ASK 1 inhibitor K811 on GC cells. K 811 efficiently prevented cell proliferation in cell lines with high ASK 1 expression and in HER 2‐overexpressing GC cells. Treatment with K 811 reduced sizes of xenograft tumors by downregulating proliferation markers. These results indicate that ASK 1 inhibition prevents GC cell growth in vitro and in vivo , suggesting that ASK 1 inhibitors can be potent therapeutic drugs for GC .

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