Faculty Profiles - FUJIWARA Toshiyoshi

MISC - FUJIWARA Toshiyoshi

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肺癌治療において遺伝子治療の目指すもの

藤原俊義, 宇野太, 香川俊輔, 片岡正文, 田中紀章

日本外科学会雑誌 103 81 - 81 2002.3

TRAIL遺伝子導入による癌細胞特異的apoptosis誘導とbystander効果

香川俊輔, 藤原俊義, 常光洋輔, 片岡正文, Fang Bingliang, 田中紀章

日本外科学会雑誌 103 127 - 127 2002.3

アデノウイルスベクターを用いたp14ARFおよびp53遺伝子導入による相乗的な抗腫瘍活性 : 作用機構とその臨床的有用性

丹後泰久, 藤原俊義, 糸島崇博, 片岡正文, 香川俊輔, 谷徹, 田中紀章

日本外科学会雑誌 103 237 - 237 2002.3

効果的なヒト細胞への遺伝子導入を目的としたレンチウイルスベクターシステムの開発

都津川敏範, 小林直哉, 興津輝, 野口洋文, 松村年久, 渡辺剛正, 丸山昌伸, 藤原俊義, 田中紀章

日本外科学会雑誌 103 527 - 527 2002.3

Activation of caspase-3 and cleavage of Rb are associated with p16-mediated apoptosis in human non-small cell lung cancer cells

K Katsuda, M Kataoka, F Uno, T Murakami, T Kondo, JA Roth, N Tanaka, T Fujiwara

ONCOGENE 21 ( 13 ) 2108 - 2113 2002.3

Language：English Publisher：NATURE PUBLISHING GROUP

The p16 tumor suppressor gene is frequently inactivated in human cancer tissues and cell lines. We previously reported that wild-type p16 expression from an adenovirus vector (Adv/p16) induced p53-dependent apoptotic cell death in non-small cell lung cancer (NSCLC) cell fines. Here we show the potential mechanism of apoptosis induced by Adv/p16 infection. Infection of human NSCLC cell line A549, which carries the wild-type p53 gene, with Adv/p16 resulted in activation of caspase-3, accompanied by the cleavage of its substrate poly (ADP-ribose) polymerase (PARP), on day 3 of infection. The retinoblastoma (Rb) cell cycle regulator protein was also cleaved after activation of caspase-3; when the levels of Rb significantly diminished, apoptosis began. When A549 cells were pretreated with the caspase-inhibitory peptide N-acetyl-asp-Glu-Val-Asp-CHO (aldehyde) (Ac-DEVD-CHO), Adv/p16-mediated apoptosis and Rb cleavage were greatly inhibited. Furthermore, MDM2, a negative regulator of p53 expression was upregulated 3 days after Adv/p16 infection, and MDM2 was subsequently cleaved by caspase-3; MDM2 cleavage was inhibited by Ac-DEVD-CHO treatment. These data implied that cleavage of Rb, in addition to activation of caspase-3, represented a mechanism by which Adv/p16 induced apoptotic cell death in human NSCLC cells. Our results support the clinical relevance of Adv/p16 as a treatment for p16-null human NSCLC that express wild-type p53.

DOI： 10.1038/sj/onc/1205272

Web of Science

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p53 inhibits adriamycin-induced down-regulation of cyclin D1 expression in human cancer cells

JH Shao, F Teraishi, K Katsuda, N Tanaka, T Fujiwara

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 290 ( 3 ) 1101 - 1107 2002.1

Language：English Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE

The tumor suppressor p53 gene product is an essential component of the cytotoxic pathway triggered by DNA-damaging stimuli such as chemotherapeutic agents and ionizing radiation. We previously demonstrated that adenovirus-mediated wild-type p53 gene transfer could enhance the cytotoxic actions of chemotherapeutic drugs both in vitro and in vivo; however, the molecular mechanism of this chemosensitization is still unclear. Cyclin D1 is a major regulator of the progression of cells into the proliferative stage of the cell cycle. Here we show that infection with an adenovirus vector expressing the wild-type p53 gene (Ad-p53) caused an increase in cyclin D1 protein levels in human colorectal cancer cell lines DLD-1 and SW620; treatment with the anti-cancer drug adriamycin, however, down-regulated their cyclin D1 protein expression in a dose-dependent manner. The suppression of cyclin D1 expression following adriamycin treatment could be blocked by simultaneous Ad-p53 infection. Furthermore, DLD-1 and SW620 cells transfected with the cyclin D1 expression construct displayed increased sensitivity to adriamycin compared to that of the vector-transfected control. Our results suggest that ectopic wild-type p53 gene transfer results in increased cyclin D1 expression and, consequently, sensitizes human colorectal cancer cells to chemotherapeutic agents. (C) 2002 Elsevier Science (USA).

DOI： 10.1006/bbrc.2001.6314

Web of Science

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Transduction of immortalized human hepatocytes with p21 to enhance differentiated phenotypes.

Kunieda T, Kobayashi N, Sakaguchi M, Okitsu T, Totsugawa T, Watanabe T, Matsumura T, Maruyama M, Noguchi H, Takesue M, Shibata N, Ohmoto K, Fujiwara T

Cell Transplant 2002

Lentiviral transfer of the LacZ gene into human endothelial cells and human bone marrow mesenchymal stem cells.

Totsugawa T, Kobayashi N, Okitsu T, Noguchi H, Watanabe T, Matsumura T, Maruyama M, Fujiwara T, Sakaguchi M, Tanaka N

Cell Transplantation 2002

Controlled expansion of human endothelial cell populations by Cre-loxP- based reversible immortalization.

Noguchi H, Kobayashi N, Westerman K A, Sakaguchi M, Okitsu T, Totsugawa T, Watanabe T, Matsumura T, Fujiwara T, Ueda T, Miyazaki M, Tanaka N, Leboulch P

Human Gene Therapy 2002

Adenovirus-Mediated p14ARF gene transfer cooperates with Ad5CMV-p53 to induce apoptosis in human cancer cells.

Tango Y, Fujiwara T, Itoshima T, Takata Y, Katsuda K, Uno F, Ohtani S, Tani T, Roth JA, Tanaka N

Human Gene Therapy 2002

Improvement in the differentiated hepatic phenotype of immortalized human hepatocytes by adenovirus mediated p21 gene transfer.

Kobayashi N, Sakaguchi M, Okitsu T, Totsugawa T, Maruyama M, Matsumura T, Watanabe T, Noguchi H, Kosaka Y, Fujiwara T, Tanaka N

Asaio J 2002

Gene therapy for cancer

FUJIWARA Toshiyoshi, TANAKA Noriaki

Nippon Nōgeikagaku Kaishi 76,4,385-387 ( 4 ) 385 - 387 2002

肺癌非手術療法の新しい試み 7.遺伝子治療.

片岡正文, 藤原俊義, 香川俊輔, 田中紀章

日本外科学会雑誌 103,2,244-249 2002

肺癌の遺伝子治療の現状と問題点.

藤原俊義, 田中紀章

臨床と研究 79,5,787-792 2002

肺癌に対する遺伝子治療：p53発現アデノウイルスベクターによる肺癌遺伝子治療臨床試験の現況.

香川俊輔, 藤原俊義, 田中紀章

医学のあゆみ 203,5,302-306 2002

p53遺伝子を用いた癌の遺伝子治療.

藤原俊義, 田中紀章

癌の臨床 48,6,303-311 2002

p53を用いた肺癌遺伝子治療.

香川俊輔, 藤原俊義, 田中紀章

日本臨床 60,Suppl 5, 630-634 2002

肺癌：局所療法としての遺伝子治療.

藤原俊義, 田中紀章

BIO Clinica 17,7,589-592 2002

レンチウイルスベクターシステム樹立に伴う安全配慮.

都津川敏範, 小林直哉, 丸山昌伸, 小坂芳和, 興津輝, 荒田尚, 阪口政清, 藤原俊義, 倉林譲, 田中紀章

Organ Biology 9,4,357-364 2002

p53遺伝子治療における抗腫瘍活性増強のストラテジー.

藤原俊義, 田中紀章

遺伝子医学 6,1,15-20 2002

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