著者 Hayashi, Tatsuro| Asano, Hiroaki| Toyooka, Shinichi| Tsukuda, Kazunori| Soh, Junichi| Shien, Tadahiko| Taira, Naruto| Maki, Yuho| Tanaka, Norimitsu| Doihara, Hiroyoshi| Nasu, Yasutomo| Huh, Nam-ho| Miyoshi, Shinichiro|
発行日 2012-05
出版物タイトル Journal of Cancer Research and Clinical Oncology
138巻
5号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/52140
フルテキストURL 68_1_23.pdf
著者 Ueno, Tsuyoshi| Toyooka, Shinichi| Fukazawa, Takuya| Kubo, Takafumi| Soh, Junichi| Asano, Hiroaki| Muraoka, Takayuki| Tanaka, Norimitsu| Maki, Yuho| Shien, Kazuhiko| Furukawa, Masashi| Sakaguchi, Masakiyo| Yamamoto, Hiromasa| Tsukuda, Kazunori| Miyoshi, Shinichiro|
抄録 The microRNA-34s (miR-34s) have p53 response elements in their 5ʼ-flanking regions and demonstrate tumor-suppressive functions. In malignant pleural mesothelioma (MPM), we previously reported that expression of miR-34b and miR-34c (miR-34b/c) was frequently downregulated by methylation in MPM cell lines and primary tumors. The forced overexpression of miR-34b/c showed significant antitumor effects with the induction of apoptosis in MPM cells. In this study, we examined the in vivo antitumor effects of miR-34b/c using adenovirus vector on MPM. We subcutaneously transplanted NCI-H290, a human MPM cell line, into BALB/C mice and injected adenovirus vector expressing miR-34b/c, luciferase driven by the cytomegalovirus promoter (Ad-miR-34b/c or Ad-Luc), or PBS control into tumors over 5mm in diameter. A statistically significant growth inhibition of the tumor volume was observed in the Ad-miR-34b/c group from day 6 onward compared to the Ad-Luc group. The inhibition rate of Ad-miR-34b/c, compared to the tumor volume treated with Ad-Luc, was 58.6% on day 10 and 54.7% on day13. Our results indicate that adenovirus-mediated miR-34b/c gene therapy could be useful for the clinical treatment of MPM.
キーワード mesothelioma microRNA microRNA-34b/c p53
Amo Type Original Article
発行日 2014-02
出版物タイトル Acta Medica Okayama
68巻
1号
出版者 Okayama University Medical School
開始ページ 23
終了ページ 26
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2014 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 24553485
Web of Sience KeyUT 000331592800004
著者 Muraoka, Takayuki| Soh, Junichi| Toyooka, Shinichi| Aoe, Keisuke| Fujimoto, Nobukazu| Hashida, Shinsuke| Maki, Yuho| Tanaka, Norimitsu| Shien, Kazuhiko| Furukawa, Masashi| Yamamoto, Hiromasa| Asano, Hiroaki| Tsukuda, Kazunori| Kishimoto, Takumi| Otsuki, Takemi| Miyoshi, Shinichiro|
発行日 2013-12
出版物タイトル Lung Cancer
82巻
3号
資料タイプ 学術雑誌論文
著者 Maki, Yuho| Soh, Junichi| Ichimura, Kouichi| Shien, Kazuhiko| Furukawa, Masashi| Muraoka, Takayuki| Tanaka, Norimitsu| Ueno, Tsuyoshi| Yamamoto, Hiromasa| Asano, Hiroaki| Tsukuda, Kazunori| Toyooka, Shinichi| Miyoshi, Shinichiro|
発行日 2013-01
出版物タイトル Oncology Reports
29巻
1号
資料タイプ 学術雑誌論文
著者 Ueno, Tsuyoshi| Tsukuda, Kazunori| Toyooka, Shinichi| Ando, Midori| Takaoka, Munenori| Soh, Junichi| Asano, Hiroaki| Maki, Yuho| Muraoka, Takayuki| Tanaka, Norimitsu| Shien, Kazuhiko| Furukawa, Masashi| Yamatsuji, Tomoki| Kiura, Katsuyuki| Naomoto, Yoshio| Miyoshi, Shinichiro|
発行日 2012-04
出版物タイトル Lung Cancer
76巻
1号
資料タイプ 学術雑誌論文
著者 Tanaka, Norimitsu| Toyooka, Shinichi| Soh, Junichi| Kubo, Takafumi| Yamamoto, Hiromasa| Maki, Yuho| Muraoka, Takayuki| Shien, Kazuhiko| Furukawa, Masashi| Ueno, Tsuyoshi| Asano, Hiroaki| Tsukuda, Kazunori| Aoe, Keisuke| Miyoshi, Shinichiro|
発行日 2012-04
出版物タイトル Lung Cancer
76巻
1号
資料タイプ 学術雑誌論文
著者 Shien, Kazuhiko| Toyooka, Shinichi| Ichimura, Kouichi| Soh, Junichi| Furukawa, Masashi| Maki, Yuho| Muraoka, Takayuki| Tanaka, Norimitsu| Ueno, Tsuyoshi| Asano, Hiroaki| Tsukuda, Kazunori| Yamane, Masaomi| Oto, Takahiro| Kiura, Katsuyuki| Miyoshi, Shinichiro|
発行日 2012-07
出版物タイトル Lung Cancer
77巻
1号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/49253
フルテキストURL 67_1_19.pdf
著者 Furukawa, Masashi| Soh, Junichi| Yamamoto, Hiromasa| Ichimura, Kouichi| Shien, Kazuhiko| Maki, Yuho| Muraoka, Takayuki| Tanaka, Norimitsu| Ueno, Tsuyoshi| Asano, Hiroaki| Tsukuda, Kazunori| Toyooka, Shinichi| Miyoshi, Shinichiro|
抄録 Nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α (NFKBIA), which is a tumor suppressor gene, was found to be silenced in lung adenocarcinomas. We examined NFKBIA expression, mutations in the EGFR and K-ras genes, and EML4-ALK fusion in 101 resected lung adenocarcinoma samples from never-smokers. NFKBIA expression was evaluated using immunohistochemistry. NFKBIA expression was negative in 16 of the 101 samples (15.8%). EGFR and K-ras mutations and EML4-ALK fusion were detected in 61 (60.5%), 1 (1.0%), and 2 (2.0%) of the 101 samples, respectively, in a completely mutually exclusive manner. Negative NFKBIA expression was observed significantly more frequently among the tumors with none of the three genetic alterations compared to those with such alterations (p=0.009). In addition, negative NFKBIA expression was significantly more frequent among the EGFR-wild type samples compared to the EGFR-mutant samples (p=0.013). In conclusion, NFKBIA expression was silenced in adenocarcinomas without EGFR/K-ras mutations or EML4-ALK fusion, suggesting that the silencing of NFKBIA may play an important role in the carcinogenesis of adenocarcinomas independent of EGFR/K-ras mutations or EML4-ALK fusion.
キーワード never-smoker lung cancer adenocarcinoma nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α epidermal growth factor receptor
Amo Type Original Article
発行日 2013-02
出版物タイトル Acta Medica Okayama
67巻
1号
出版者 Okayama University Medical School
開始ページ 19
終了ページ 24
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2013 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 23439505
Web of Sience KeyUT 000316829900003
関連URL http://ousar.lib.okayama-u.ac.jp/metadata/52534
JaLCDOI 10.18926/AMO/46629
フルテキストURL 65_3_179.pdf
著者 Teramen, Hirotake| Tsukuda, Kazunori| Tanaka, Norimitsu| Ueno, Tsuyoshi| Kubo, Takafumi| Ando, Midori| Soh, Junichi| Asano, Hiroaki| Pass, Harvery I.| Toyooka, Shinichi| Miyoshi, Shinichiro|
抄録 Suppression of p21 has been implicated in the genesis and progression of many human malignancies. DNA methylation is an important mechanism of gene silencing in human malignancies. In this study, we examined the expression status and aberrant methylaion of p21 in lung cancers and malignant pleural mesotheliomas (MPM). We used 12 small cell lung cancer (SCLC) cell lines, 13 non-small cell lung cancer (NSCLC) cell lines, 50 primary NSCLCs, 6 MPM cell lines and 10 primary MPMs. The expression and methylation of p21 was examined by reverse transcription-PCR (RT-PCR), Western blotting and methylation-specific PCR (MSP) assay. Loss of p21 protein expression was observed in 7 SCLC cell lines (58.3%), 5 NSCLC cell lines (38.5%) and 3 MPM cell lines (50%) while mRNA expression was lost in 2 SCLC cell lines (16.7%), 2 NSCLC cell lines (15.4%) and none of the MPM cell lines. Aberrant methylation of p21 was found in 8.3% of SCLC cell lines, 30.2% of NSCLCs and 6.3% of MPMs. Among primary NSCLCs, methylation in adenocarcinomas was significantly more frequent than in squamous cell carcinomas. Loss of p21 expression was frequently observed in lung cancers and MPMs and aberrant methylation was one of the mechanisms of suppression of p21, especially in NSCLCs.
キーワード p21 methylation lung cancer mesothelioma
Amo Type Original Article
発行日 2011-06
出版物タイトル Acta Medica Okayama
65巻
3号
出版者 Okayama University Medical School
開始ページ 179
終了ページ 184
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2011 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 21709715
Web of Sience KeyUT 000292017500004