2019 Fiscal Year Final Research Report

Identifying new therapeutic target using transcribed ultra-conserved region related to androgen receptor in prostate cancer

Research Project

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Project/Area Number	17K11140
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Urology
Research Institution	Hiroshima University
Principal Investigator	Hieda Keisuke 広島大学, 病院(医), 助教 (60625630)
Co-Investigator(Kenkyū-buntansha)	松原昭郎広島大学, 医系科学研究科(医), 教授 (10239064) 亭島淳広島大学, 医系科学研究科(医), 准教授 (20397962) 安井弥広島大学, 医系科学研究科(医), 教授 (40191118) 池田健一郎広島大学, 病院(医), 助教 (50624863) 林哲太郎広島大学, 医系科学研究科(医), 助教 (60612835)
Project Period (FY)	2017-04-01 – 2020-03-31
Keywords	前立腺癌 / バイオマーカー / ドセタキセル
Outline of Final Research Achievements	Overexpression of Uc.63+ promoted docetaxel (DTX) resistance in LNCaP cells. On the contrary, knockdown of Uc.63+ had no effect on DTX resistance in PC3 and DU145 which are well known AR negative prostate cancer (PCa) cell lines. These results suggest that Uc.63+ may be involved in DTX resistance.The serum expression of Uc.63+ was higher in metastatic PCa than that in primary PCa. We analysed the role of Uc.63+ as biomarker for DTX treatment. The serum expression of Uc.63+ was higher in patient with resistance to DTX than that in patients with favourable response to DTX. Kaplan-meier analysis showed that high Uc.63+ expression was associated with poor overall survival.
Free Research Field	前立腺癌
Academic Significance and Societal Importance of the Research Achievements	去勢抵抗性前立腺癌においてドセタキセルはlst line治療として確立しているが、その奏効率は60-70％程度であり、無効症例が存在するため、治療効果予測マーカーの開発が求められる。今回、転写超保存領域であるUc.63+が高値群においてドセタキセル治療抵抗であり、さらに予後が悪いことを明らかにした。ドセタキセル治療における治療効果予測マーカーとしての可能性について今後、研究を継続していく。