| Author | 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| |
|---|---|
| Published Date | 2012-05 |
| Publication Title | Journal of Cancer Research and Clinical Oncology |
| Volume | volume138 |
| Issue | issue5 |
| Content Type | Journal Article |
| JaLCDOI | 10.18926/AMO/52140 |
|---|---|
| FullText URL | 68_1_23.pdf |
| Author | 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| |
| Abstract | 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. |
| Keywords | mesothelioma microRNA microRNA-34b/c p53 |
| Amo Type | Original Article |
| Publication Title | Acta Medica Okayama |
| Published Date | 2014-02 |
| Volume | volume68 |
| Issue | issue1 |
| Publisher | Okayama University Medical School |
| Start Page | 23 |
| End Page | 26 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | CopyrightⒸ 2014 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 24553485 |
| Web of Science KeyUT | 000331592800004 |
| Author | 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| |
|---|---|
| Published Date | 2013-12 |
| Publication Title | Lung Cancer |
| Volume | volume82 |
| Issue | issue3 |
| Content Type | Journal Article |
| Author | 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| |
|---|---|
| Published Date | 2013-01 |
| Publication Title | Oncology Reports |
| Volume | volume29 |
| Issue | issue1 |
| Content Type | Journal Article |
| Author | 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| |
|---|---|
| Published Date | 2012-04 |
| Publication Title | Lung Cancer |
| Volume | volume76 |
| Issue | issue1 |
| Content Type | Journal Article |
| Author | 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| |
|---|---|
| Published Date | 2012-04 |
| Publication Title | Lung Cancer |
| Volume | volume76 |
| Issue | issue1 |
| Content Type | Journal Article |
| Author | 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| |
|---|---|
| Published Date | 2012-07 |
| Publication Title | Lung Cancer |
| Volume | volume77 |
| Issue | issue1 |
| Content Type | Journal Article |
| JaLCDOI | 10.18926/AMO/49253 |
|---|---|
| FullText URL | 67_1_19.pdf |
| Author | 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| |
| Abstract | 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. |
| Keywords | 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 |
| Publication Title | Acta Medica Okayama |
| Published Date | 2013-02 |
| Volume | volume67 |
| Issue | issue1 |
| Publisher | Okayama University Medical School |
| Start Page | 19 |
| End Page | 24 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | CopyrightⒸ 2013 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 23439505 |
| Web of Science KeyUT | 000316829900003 |
| Related Url | http://ousar.lib.okayama-u.ac.jp/metadata/52534 |
