Ultraconserved long non-coding RNA uc.63 in breast cancer
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Alberto Marini1, Anna Maria Lena2, Emanuele Panatta2, Cristina Ivan3, Leng Han4, Han Liang5, Margherita Annicchiarico-Petruzzelli6, Nicola Di Daniele2, George A. Calin3, Eleonora Candi2,6 and Gerry Melino1,2
1Medical Research Council, Toxicology Unit, Hodgkin Building, University of Leicester, Leicester, UK
2Department of Experimental Medicine and Surgery, University of Rome “Tor Vergata”, Rome, Italy
3Department of Experimental Therapeutics and The Center for RNA interference and non-coding RNA, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA
4Department of Biochemistry and Molecular Biology, The University of Texas Health Science Center at Houston McGovern Medical School, Houston, TX, USA
5Department of Bioinformatics and Computational Biology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA
6IDI-IRCCS, Biochemistry Laboratory, Rome, Italy
George A. Calin, email: firstname.lastname@example.org
Eleonora Candi, email: email@example.com
Gerry Melino, email: firstname.lastname@example.org
Keywords: lncRNA, T-UCRs, breast cancer, apoptosis, prognosis
Received: March 30, 2016 Accepted: May 13, 2016 Published: July 13, 2016
Transcribed-ultraconserved regions (T-UCRs) are long non-coding RNAs (lncRNA) encoded by a subset of long ultraconserved stretches in the human genome. Recent studies revealed that the expression of several T-UCRs is altered in cancer and growing evidences underline the importance of T-UCRs in oncogenesis, offering also potential new strategies for diagnosis and prognosis. We found that overexpression of one specific T-UCRs named uc.63 is associated with bad outcome in luminal A subtype of breast cancer patients. uc.63 is localized in the third intron of exportin-1 gene (XPO1) and is transcribed in the same orientation of its host gene. Interestingly, silencing of uc.63 induces apoptosis in vitro. However, silencing of host gene XPO1 does not cause the same effect suggesting that the transcription of uc.63 is independent of XPO1. Our results reveal an important role of uc.63 in promoting breast cancer cells survival and offer the prospect to identify a signature associated with poor prognosis.
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