2019 Fiscal Year Final Research Report
Elucidate the functional RNA network in castration-resistant prostate cancer and therapeutic approach
Project/Area Number |
17K11160
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Urology
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Research Institution | Teikyo University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
関 直彦 千葉大学, 大学院医学研究院, 准教授 (50345013)
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Project Period (FY) |
2017-04-01 – 2020-03-31
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Keywords | マイクロRNA / 去勢抵抗性前立腺癌 / 抗がん剤 / ホルモン感受性 / 癌遺伝子 |
Outline of Final Research Achievements |
Tumor suppressor genes induce up-regulation of oncogenes, which promote aggressiveness of castration-resistant prostate cancer (CRPC). Micro-RNAs repress expression of target genes, especially oncogenes in CRPC. To find out oncogenes which have important roles in progression of CRPC makes us possible to inhibit progression, invasion, and metastasis in CRPC. We previously reported that miR-455-5p is down-regulated in progressive PCa. We have found out the 8 possible target genes of miR-455-5p. The expression levels of Pirin was most increased in CRPC and the expression levels are repressed by miR-455-5p. miR-455-5p might a prognositic factor of progressed PCa and inhibition of expression of Pirin might be a therapeutic strategy in progressed PCa and CRPC.
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Free Research Field |
前立腺癌
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Academic Significance and Societal Importance of the Research Achievements |
ホルモン療法に抵抗性となった去勢抵抗性前立腺癌(CRPC)は予後が約2年から5年と予後には限りがある。前立腺癌の進展のメカニズムは色々な仮説があるが、本研究では、癌遺伝子の発現を調節するマイクロRNAを同定し、その標的遺伝子を明らかにした。マイクロRNAを強発現させることで、前立腺癌の増殖や転移を抑える可能性があることから、将来的な治療への応用することができるかもしれない。
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