| Project/Area Number |
17K11165
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | Kindai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
植村 天受 近畿大学, 医学部, 教授 (90213397)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 前立腺癌 / ノンコーディングRNA / バイオマーカー / 遺伝子改変マウスモデル / バイオマーカ / PTENノックアウト / 腫瘍免疫 / トランスクリプトーム解析 |
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| Outline of Final Research Achievements |
We previously showed that androgen withdrawal led to increased alternatively spliced products in our originally established mouse prostate tumors. Here, we perform gene expression analysis this mouse prostate cancer model to identify candidate mRNA processing genes implicated in the progression to castration-resistant disease. Affymetrix GeneChip mouse transcriptome assay to perform comparative analysis of the transcriptomes of normal prostate tissue and PTEN-deficient castration-naïve, castration-sensitive prostate cancers. Clustering analysis revealed genes enriched with the functions involved in mRNA splicing and processing in mice with prostate tumors. Of these. We focused on NEAT1（encoding nuclear paraspeckle assembly transcript 1）and investigated anti-tumor effects using our mouse prostate cancer model. A part of the date was reported at JCA and AACR meetings.
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| Academic Significance and Societal Importance of the Research Achievements |
我々が開発した前立腺癌マウスモデルは、ヒト前立腺癌の自然史と同様の発生・進展を示し、CRPCモデルにおいてもAR発現プロファイルが酷似していることから、様々な前臨床試験での検証を可能にしてきただけでなく、分子レベルの基礎研究を飛躍的に転換させるものである。今回の新たなアプローチで同定される新規標的分子をスピーディーに検証できる意義は大きく、知的財産等につながることができれば医学的に極めて重要なメリットとなるであろう。
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