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ID 49034
フルテキストURL
著者
Nakanishi, Yutaka Okayama Univ
Shiraha, Hidenori Okayama Univ
Nishina, Shin-ichi Okayama Univ
Tanaka, Shigetomi Okayama Univ
Matsubara, Minoru Okayama Univ
Horiguchi, Shigeru Okayama Univ
Iwamuro, Masaya Okayama Univ
Takaoka, Nobuyuki Okayama Univ
Uemura, Masayuki Okayama Univ
Kuwaki, Kenji Okayama Univ
Hagihara, Hiroaki Okayama Univ
Toshimori, Junichi Okayama Univ
Ohnishi, Hideki Okayama Univ
Takaki, Akinobu Okayama Univ
Nakamura, Shinichiro Okayama Univ
Kobayashi, Yoshiyuki Okayama Univ
Nouso, Kazuhiro Okayama Univ
Yagi, Takahito Okayama Univ
Yamamoto, Kazuhide Okayama Univ
抄録
Background: Runt-related transcription factor 3 (RUNX3) is known as a tumor suppressor gene for gastric cancer and other cancers, this gene may be involved in the development of hepatocellular carcinoma (HCC). Methods: RUNX3 expression was analyzed by immunoblot and immunohistochemistry in HCC cells and tissues, respectively. Hep3B cells, lacking endogenous RUNX3, were introduced with RUNX3 constructs. Cell proliferation was measured using the MTT assay and apoptosis was evaluated using DAPI staining. Apoptosis signaling was assessed by immunoblot analysis. Results: RUNX3 protein expression was frequently inactivated in the HCC cell lines (91%) and tissues (90%). RUNX3 expression inhibited 90 +/- 8% of cell growth at 72 h in serum starved Hep3B cells. Forty-eight hour serum starvation-induced apoptosis and the percentage of apoptotic cells reached 31 +/- 4% and 4 +/- 1% in RUNX3-expressing Hep3B and control cells, respectively. Apoptotic activity was increased by Bim expression and caspase-3 and caspase-9 activation. Conclusion: RUNX3 expression enhanced serum starvation-induced apoptosis in HCC cell lines. RUNX3 is deleted or weakly expressed in HCC, which leads to tumorigenesis by escaping apoptosis.
発行日
2011-01-04
出版物タイトル
BMC Cancer
11巻
ISSN
1471-2407
資料タイプ
学術雑誌論文
オフィシャル URL
http://dx.doi.org/10.1186/1471-2407-11-3
言語
English
論文のバージョン
publisher
査読
有り
DOI
Web of Sience KeyUT