Identification of miRNA and its target gene by proteome analysis in hormone refractory prostate cancer

激素难治性前列腺癌蛋白质组分析鉴定miRNA及其靶基因

• 批准号: 23791798
• 负责人: ISHIGURO Hitoshi
• 金额: $ 2.75万
• 依托单位: 公益財団法人神奈川科学技術アカデミー (2012)Kanagawa Academy of Science and Technology (2011)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23791798/
• 关键词: 腫瘍学; miRNA; 再燃; 前立腺癌

micro RNAs (miRNAs) regulate many genes and therefore their expression abnormality cause various diseases including cancer. Previously, we identified some miRNAs that might be related with prostate cancer progression. In this study, we found that miR-30d expression in cancer cells and tissues is higher than in normal prostate cells and tissues. Further, miR-30d expression was associated with recurrence free survival ratio. Therefore miR-30d might be a prognosis factor for prostate cancer recurrence. We identified that SOCS1 was one of the targets for miR-30d. SOCS1 regulation by miR-30 was related with prostate cancer progression.

微小RNA（microRNAs，miRNAs）调控着许多基因，其表达异常导致包括癌症在内的多种疾病。在此之前，我们发现了一些可能与前列腺癌进展相关的miRNAs。在本研究中，我们发现miR-30 d在癌细胞和组织中的表达高于正常前列腺细胞和组织。此外，miR-30 d表达与无复发生存率相关。因此，miR-30 d可能是前列腺癌复发的一个预后因子。我们确定SOCS 1是miR-30 d的靶点之一。miR-30对SOCS 1的调控与前列腺癌进展相关。

项目成果

miR-30d promotes prostate cancer progression and associated with early biochemical recurrence

miR-30d 促进前列腺癌进展并与早期生化复发相关

• 发表时间: 2012
• 作者: 古林直人;上村博司;奥寺康司;稲山嘉明;青木一郎;窪田吉信;長嶋洋治;石黒斉
• 通讯作者: 石黒斉

Identification of miR-30d as a novel prognostic maker of prostate cancer.

• DOI: 10.18632/oncotarget.696
• 发表时间: 2012-11
• 期刊: Oncotarget
• 作者: Kobayashi N;Uemura H;Nagahama K;Okudela K;Furuya M;Ino Y;Ito Y;Hirano H;Inayama Y;Aoki I;Nagashima Y;Kubota Y;Ishiguro H
• 通讯作者: Ishiguro H

Overexpression of miR-30d modulates cancer progression through the downregulation of SOCS1

miR-30d 的过表达通过 SOCS1 的下调调节癌症进展

• 发表时间: 2012
• 作者: Kobayashi N;Uemura H;Nagahama N;Okudela K;Furuya M;Ino Y;Ito Y;Hirano H;Inayama Y;Aoki I;Nagashima Y;Kubota Y;Ishiguro H.
• 通讯作者: Ishiguro H.