Pyrrole‐imidazole polyamide targeted to break fusion sites in TMPRSS2 and ERG gene fusion represses prostate tumor growth. Issue 10 (18th September 2014)

• Record Type: Journal Article
• Authors: Obinata, Daisuke; Ito, Akiko; Fujiwara, Kyoko; Takayama, Ken‐Ichi; Ashikari, Daisaku; Murata, Yasutaka; Yamaguchi, Kenya; Urano, Tomohiko; Fujimura, Tetsuya; Fukuda, Noboru; Soma, Masayoshi; Watanabe, Takayoshi; Nagase, Hiroki; Inoue, Satoshi; Takahashi, Satoru
• Is Part Of: Cancer science. Volume 105:Issue 10(2014:Oct.)
• Page Start: 1272
• Page End: 1278
• Publication Date: 2014-09-18
• Subjects: Cancer -- Periodicals; Neoplasms -- Periodicals; Research -- Periodicals; Electronic journals; 616.994005
• DOI: 10.1111/cas.12493
• Languages: English
• ISSNs: 1347-9032

Abstract

<abstract abstract-type="main" id="cas12493-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Aberrant overexpression of ERG induced by the <italic>TMPRSS2‐ERG</italic> gene fusion is likely involved in the development of prostate cancer. Synthetic pyrrole–imidazole (PI) polyamides recognize and attach to the minor groove of DNA with high affinity and specificity. In the present study, we designed a PI polyamide targeting <italic>TMPRSS2‐ERG</italic> translocation breakpoints and assessed its effect on human prostate cancer cells. Our study identified that this PI polyamide repressed the cell and tumor growth of androgen‐sensitive LNCaP prostate cancer cells. Targeting of these breakpoint sequences by PI polyamides could be a novel approach for the treatment of prostate cancer.</p> </abstract>