Abstract 5042: A-AS1 , a long non-protein coding RNA overexpressed in esophageal adenocarcinoma, influences cancer cell proliferation and apoptosis

• Published in: Cancer research (Chicago, Ill.) Vol. 72; no. 8_Supplement; p. 5042
• Main Authors: Wu, Wenjing, Song, Jee Hoon, Cheng, Yulan, Meltzer, Stephen J.
• Format: Journal Article
• Language: English
• Published: 15.04.2012
• ISSN: 0008-5472; 1538-7445
• DOI: 10.1158/1538-7445.AM2012-5042

Abstract Esophageal adenocarcinoma (EAC) is one of the fastest-growing cancers in the Western world. 95% of EACs occur without any antecedent diagnosis of Barrett's esophagus (BE). In these 95% of EAC patients, 5-year survival is only 15%. The rising incidence and poor prognosis of EAC have intensified research efforts into earlier methods to detect this disease. The majority of the human genome is transcribed and generates mostly non-coding (nc)RNAs that do not encode protein information. Long non-coding RNAs (lncRNAs) are emerging as a novel class of ncRNAs, but knowledge about these ncRNAs is limited. Recently, dysregulation of lncRNAs has been shown in various types of cancer, suggesting that lncRNAs may be involved in tumorigenesis or tumor progression. In the present study, we report that a number of lncRNAs are differentially expressed in EAC tissues and cell lines relative to normal esophageal tissues and cell lines. One of these lncRNAs, A-AS1 is derived from the antisense strand of the A gene locus and is overexpressed in EACs relative to matched normal esophagus (NE). Cell proliferation and colony formation assays revealed that A-AS1 siRNA-mediated knockdown reduces cell proliferation and colony-forming ability. In vitro scratch assays, migration and invasion assays in vitro also demonstrated decreased migration and invasion induced by A-AS1 siRNA knockdown. Moreover, we found that inhibition of A-AS1 expression results in increased apoptosis in EAC cell lines. Taken together, these results suggest that the elevated expression of A-AS1 observed in EACs may have contributed to their development or progression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5042. doi:1538-7445.AM2012-5042