P-025 - Long non-coding RNA AOC4P suppressed hepatocellular carcinoma metastasis by inhibiting epithelial-mesenchymal transition

Date 04 July 2015
Event WorldGI 2015
Session Posters
Topics Hepatobiliary Cancers
Translational Research
Basic Principles in the Management and Treatment (of cancer)
Presenter T.-H. Wang
Citation Annals of Oncology (2015) 26 (suppl_4): 1-100. 10.1093/annonc/mdv233
Authors T.-. Wang, Y.-. Lin, C.-. Yeh, T.-. Chen
  • Chang Gung Memorial Hospital, Tao-Yuan/TW



Recently, increasing evidence indicates that long noncoding RNAs (lncRNAs) play a critical role in the regulation of diverse cellular processes such as cell growth, differentiation, cell cycle progression, and apoptosis. Additionally, several lncRNAs are frequently aberrantly expressed in various human cancers, with both oncogenic and tumor suppressive potential roles. Nevertheless, just a few reports addressed the role of lncRNAs in hepatocellular carcinoma (HCC) progression. In this study, we tried to identify and characterize the role of lncRNA-AOC4P in the regulation of hepatocarcinogenesis.


The expression level of AOC4P was examined in 121 paired HCC and para-tumoral liver tissues using quantitative real-time RT-PCR. The correlation between AOC4P levels, clinical parameters, and survival outcomes were analyzed to elucidate the clinical significance of AOC4P in HCC. In vitro and in vivo functional assays were also performed to dissect the underlying mechanisms.


The expression of AOC4P was significantly downregulated in HCC tissues and low expression of AOC4P correlated with poor prognostic outcomes. Furthermore, in vitro functional assays indicated that AOC4P significantly reduced cell proliferation, migration and invasion ability through inhibiting epithelial-mesenchymal transition. The in vivo animal model also demonstrated the tumor suppressor role of AOC4P via reducing tumor growth and metastasis.


AOC4P may act as a tumor suppressor in HCC by reduced cell proliferation, migration and invasion ability through suppressing epithelial-mesenchymal transition. The findings could help us to further understand the mechanism of HCC progression and to develop new therapeutic strategies for HCC.