Study of the mechanisms of cancer prevention by food factors for personalized prevention

研究食物因素防癌机制，实现个体化预防

• 批准号: 16590479
• 负责人: SOWA Yoshihiro
• 金额: $ 2.18万
• 依托单位: Kyoto Prefectural University of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2004
• 资助国家: 日本
• 起止时间: 2004 至 2005
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-16590479/
• 关键词: cancer prevention; food factor; genistein; apigenin; fucoxantin; artepillin C; sulforaphane; molecular-targeting cancer prevention; がん予防; p21; WAF1; DR5; TRAIL; ゲニステイン; アピゲニン; p53; G2; M期; Gadd45; CCAAT; NF-Y

As for the relation between cancer and the meal, implications are suggested as a cancer prevention factor there are a lot of uncertain points of the action mechanism of the cancer prevention though it is reported that a variety of cancer prevention factors are actually included in food. Then, the research that clarified the action mechanism was executed to the food factor from which the cancer prevention effect was reported.We studied the action mechanisms of genistein, that is flavonoid included in the soybeans, apigenin, that is also flavonoid included in green vegetables, fucoxantin, that is natural carotenoid included in seaweeds, artepillin C, that is an element of bee products, propolis, and sulforaphane, that is isothiocyanate such as isothiocyanate sulforaphane included in crucifer vegetables.Genistein inhibited the proliferation of the cancer cell by inducing the gadd45 gene. Apigenin inhibited the proliferation of the cancer cell by inducing the p21/WAF1 gene. Both fucoxantin and artepillin C also induced the p21/WAF1 gene and inhibited the proliferation of the cancer cell.These results suggest the possibility of the development of the molecular target cancer preventive that makes gadd45 and p21/WAF1 target molecules. We found that the sulforaphane induced DR5 that is the receptor molecule of TRAIL that was the apoptosis inducible cytokine. As the result, apoptosis is enabled to be induced to the cancer cell by the low concentration of TRAIL treatment in inducing DR5 by sulforaphane, and these results suggest the development of the molecular-targeting combination cancer preventive using together of sulforaphane and TRAIL that makes DR5 target molecule.

对于癌症与膳食的关系，建议暗示作为一种预防癌症的因素，尽管有报道称食物中实际上含有多种预防癌症的因素，但其预防癌症的作用机制仍有很多不确定之处。然后，对报道其防癌作用的食物因素进行了澄清作用机制的研究。我们研究了大豆中的黄酮类染料木素、绿色蔬菜中的黄酮类蔬菜素、海藻中的天然类胡萝卜素、蜂产品中的青蒿素C、十字花科蔬菜中的异硫氰酸盐萝卜硫素等萝卜硫素的作用机制。染料木素通过诱导gadd45基因抑制癌细胞的增殖。芹菜素通过诱导p21/WAF1基因抑制癌细胞的增殖。岩藻黄嘌呤和青蒿素C均能诱导p21/WAF1基因表达，抑制癌细胞的增殖。这些结果提示了开发以gadd45和p21/WAF1为靶标分子的靶向癌症预防分子的可能性。我们发现萝卜硫素诱导DR5，即TRAIL的受体分子，是细胞凋亡诱导因子。结果表明，在萝卜硫素诱导DR5的过程中，低浓度的TRAIL处理可诱导癌细胞凋亡，提示萝卜硫素与TRAIL联合使用，使DR5成为靶分子的分子靶向联合防癌方法的发展。

项目成果

HDAC3 and other class I HDACs regulate colon cell maturation and p21 expression, and are deregulated in human colon cancer.

HDAC3 和其他 I 类 HDAC 调节结肠细胞成熟和 p21 表达，并且在人类结肠癌中失调。

• 发表时间: 2006
• 期刊: Journal Biological Chemistry (印刷中)
• 作者: Yoshikazu Miura;Hisao Matsui;Wilson AJ. et al.
• 通讯作者: Wilson AJ. et al.

Aaptamine, a spongean alkaloid, activates p21 promoter in a p53-independent manner

• DOI: 10.1016/j.bbrc.2006.01.119
• 发表时间: 2006-03-31
• 期刊: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
• 影响因子: 3.1
• 作者: Aoki, S;Kong, DX;Kobayashi, M
• 通讯作者: Kobayashi, M

Apigenin induces cell cycle arrest and p21/WAF1 expression in a p53-independent pathway.

• DOI: 10.3892/ijo.26.1.185
• 发表时间: 2005
• 期刊: International journal of oncology
• 影响因子: 5.2
• 作者: Nobumasa Takagaki;Y. Sowa;Teruki Oki;Ryoko Nakanishi;Shingo Yogosawa;T. Sakai

A new cancer diagnostic system based on a CDK profiling technology

• DOI: 10.1016/j.bbadis.2005.06.001
• 发表时间: 2005-09-25
• 期刊: BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
• 影响因子: 6.2
• 作者: Ishihara, H;Yoshida, T;Sakai, T
• 通讯作者: Sakai, T

Artepillin C in Brazilian propolis induces G0/G1 arrest via stimulation of Cip1/p21 expression in human colon cancer cells

• DOI: 10.1002/mc.20148
• 发表时间: 2005-12-01
• 期刊: MOLECULAR CARCINOGENESIS
• 影响因子: 4.6
• 作者: Shimizu, K;Das, SK;Kanazawa, K
• 通讯作者: Kanazawa, K