Journal
INTERNATIONAL JOURNAL OF ONCOLOGY
Volume 42, Issue 6, Pages 2087-2093Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ijo.2013.1898
Keywords
imiquimod; prostate cancer; apoptosis; cell cycle arrest
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Funding
- program for Basic Research in Science and Engineering [2010-0002626]
- World Class Institute (WCI) program of the National Research Foundation of Korea (NRF) [2009-002]
- Ministry of Education, Science and Technology of Korea (MEST)
- Korea Evaluation Institute of Industrial Technology (KEIT) [2009-002] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Prostate cancer is the second leading cause of cancer death in men worldwide. In the present study, we examined in vitro and in vivo antitumor effect of the small molecule imiquimod, also known as a TLR7 agonist, against prostate cancer. Imiquimod inhibited the growth of mouse (TRAMP-C2) and human (PC-3) prostate cancer cells. Treatment with imiquimod induced cell cycle arrest at the G(2)/M phase in TRMPA-C2 cells, confirmed by the changes of G(2)/M checkpoint regulators such as reduction of cyclin B1 expression and increase of phospho-CDC2 and p21 in TRAMP-C2 cells treated with imiquimod. Flow cytometry and western blot analysis revealed that imiquimod induced direct apoptosis in TRAMP-C2 cells via a mitochondrial-dependent pathway. Intratumoral injection with imiquimod reduced significantly tumor growth and increased apoptotic cells in mice subcutaneously implanted with TRAMP-C2 cells. Our results indicate that imiquimod can be an alternative therapeutic for locally generated prostate cancer.
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