Regulation of cancer progression by PICT1 and development of cancer therapeutics

2014 Fiscal Year Final Research Report

• Project/Area Number: 23592132
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cerebral neurosurgery
• Research Institution: Kagoshima University (2012-2014); Kyushu University (2011)
• Principal Investigator: KAWAHARA KOHICHI 鹿児島大学, 医歯(薬)学総合研究科, 講師 (00400482)
• Project Period (FY): 2011-04-28 – 2015-03-31
• Keywords: 核小体ストレス応答 / p53 / がん / 細胞増殖 / 抗癌剤 / レポーターシステム / 薬剤スクリーニング

Outline of Final Research Achievements

Nucleolar stress response is a newly identified mechanism which regulates tumor suppressor p53 protein. We previously identified PICT1 as a novel key regulator of nucleolar stress response. In the present study, we investigated tumor regulatory function of PICT1. We found reduced PICT1 expression decreased cancer cell growth and accumulated p53. In addition, we showed low PICT1 expression associated with better prognosis in cancer patients. These observation suggested that the nucleolar stress response PICT1 regulates could play a definitive role in tumor suppression and, chemicals which induce nucleolar stress response might be attractive cancer therapeutics. Then, we next constructed a reporter system to visualize and quantitate nucleolar stress response. We found that this reporter system allowed quantitative measurement with excellent accuracy. This reporter system may lead to identify novel cancer therapeutics.

Free Research Field

分子腫瘍学