Can the regulation of autophagy be a new target for the treatment of prostate cancer?

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592383
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: University of Fukui
• Principal Investigator: ITO HIDEAKI 福井大学, 医学部附属病院, 講師 (00345620)
• Co-Investigator(Kenkyū-buntansha): TAGA Minekatsu 福井大学, 医学部附属病院, 助教 (00529349) ; YOKOYAMA Osamu 福井大学, 医学部, 教授 (90242552) ; TSUCHIYAMA Katsuki 福井大学, 医学部附属病院, 助教 (90464073) ; INAMURA Sou 福井大学, 医学部付属病院, 医員 (50572434)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 腫瘍学

Outline of Final Research Achievements

Temsirolimus (TEM) induced autophagy but did not induce apoptosis even in high-dose treatment. The combination of low-dose docetaxel (DTX) and TEM caused a 34% suppression of cell proliferation compared to monotherapy with a higher dose in both the PC3 and LNCaP cells. The induction of apoptosis was increased in the DTX + TEM combination group compared to the monotherapy groups. The combination with low-dose DTX, which did not induce apoptosis by monotherapy, off-set the induction of autophagy by TEM, which indicates that-DTX suppressed the TEM-induced autophagy. The combination treatment suppressed tumor growth to 72 % less than the control group 14 days after the initial treatment in vivo.
In the combination therapy, DTX induced apoptosis by overcoming the autophagy induced by TEM and enhanced the effect of suppression of cell proliferation.

Free Research Field

医歯薬学