| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2017-10-05 |
| タイトル |
|
|
タイトル |
α-Lipoic acid-induced inhibition of proliferation and met phosphorylation in human non-small cell lung cancer cells |
| 言語 |
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|
言語 |
eng |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| ID登録 |
|
|
ID登録 |
10.24517/00027451 |
|
ID登録タイプ |
JaLC |
| 著者 |
Michikoshi, Hiromitsu
Nakamura, Takahiro
Sakai, Katsuya
Suzuki, Yoshinori
Adachi, Eri
Matsugo, Seiichi
松本, 邦夫
|
| 著者別表示 |
中村, 隆弘
酒井, 克也
松郷, 誠一
松本, 邦夫
|
| 提供者所属 |
|
|
内容記述タイプ |
Other |
|
内容記述 |
金沢大学がん進展制御研究所 |
| 書誌情報 |
Cancer Letters
巻 335,
号 2,
p. 472-478,
発行日 2013-07-28
|
| ISSN |
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収録物識別子タイプ |
ISSN |
|
収録物識別子 |
0304-3835 |
| NCID |
|
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収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA00598513 |
| DOI |
|
|
関連タイプ |
isVersionOf |
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
10.1016/j.canlet.2013.03.008 |
| 出版者 |
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出版者 |
Elsevier |
| 抄録 |
|
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内容記述タイプ |
Abstract |
|
内容記述 |
α-Lipoic acid (α-LA), a naturally occurring anti-oxidant and co-factor for metabolic enzymes, suppresses the growth of different types of tumor cells. The mechanisms that are responsible for these results, however, remain to be elucidated. In the present study, we investigated the effects of α-LA on the proliferation and activation status of definitive receptor tyrosine kinases, epidermal growth factor receptor (EGFR) and Met/hepatocyte growth factor (HGF) receptor, in gefitinib-sensitive human non-small cell lung cancer cells harboring EGFRs with an activating mutation. The enantiomers R-α-LA and S-α-LA suppressed cell proliferation and increased the level of reactive oxygen species in HCC-827 and PC-9 human non-small cell lung cancer cells in an indistinguishable dose-dependent fashion. A phospho-receptor tyrosine kinase array and cell cycle analysis indicated that α-LA decreased tyrosine phosphorylation levels of EGFR, ErbB2, and Met, and this was associated with an inhibition in the cell-cycle transition from the G1 phase to the S phase without inducing apoptosis. Gefitinib, an inhibitor for EGFR tyrosine kinase, inhibited EGFR tyrosine phosphorylation/activation and proliferation of the cells. Instead, the addition of HGF induced Met tyrosine phosphorylation, and this was associated with a resistance to gefitinib-induced growth inhibition, which meant a gain in proliferative ability. In the presence of gefitinib and HGF, the addition of α-LA suppressed Met tyrosine phosphorylation, and this was associated with an inhibition in cell growth. These results suggest that the suppression of tyrosine phosphorylation/activation of growth factor receptors that is critical for the proliferation of human non-small cell lung cancer cells is a mechanism by which α-LA exerts growth inhibition for cancer cells. © 2013 Elsevier Ireland Ltd. All rights reserved. |
| 権利URI |
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|
権利情報 |
http://www.elsevier.com/locate/issn/03043835 |
| 著者版フラグ |
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|
出版タイプ |
AM |
|
出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
SC-PR-MATSUMOTO-K-472.pdf (580.7 kB)
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