Transcriptome profiling identifies a recurrent CRYL1-IFT88 chimeric transcript in hepatocellular carcinoma
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Yi Huang1,2,*, Jiaying Zheng1,2,*, Dunyan Chen1,2, Feng Li1,3, Wenbing Wu1,2, Xiaoli Huang1,2, Yanan Wu1,2, Yangyang Deng4 and Funan Qiu1,5
1Provincial Clinical College, Fujian Medical University, Fuzhou 350001, Fujian, China
2Department of Clinical Laboratory, Fujian Provincial Hospital, Fuzhou 350001, Fujian, China
3Department of Pathology, Fujian Provincial Hospital, Fuzhou 350001, Fujian, China
4Department of Bioinformatics, MyGene Diagnostics Co., Ltd, Guangzhou 510300, Guangdong, China
5Department of Hepatobiliary Surgery, Fujian Provincial Hospital, Fuzhou 350001, Fujian, China
*These authors contributed equally to this work
Funan Qiu, email: [email protected]
Yi Huang, email: [email protected]
Keywords: HCC, transcriptome sequencing, fusion transcript, CRYL1-IFT88, tumorigenesis
Received: January 28, 2017 Accepted: April 05, 2017 Published: April 19, 2017
We performed transcriptome sequencing for hepatocellular carcinoma (HCC) and adjacent non-tumorous tissues to investigate the molecular basis of HCC. Nine HCC patients were recruited and differentially expressed genes (DEGs) were identified. Candidate fusion transcripts were also identified. A total of 1943 DEGs were detected, including 690 up-regulated and 1253 down-regulated genes, and enriched in ten pathways including cell cycle, DNA replication, p53, complement and coagulation cascades, etc. Seven candidate fusion genes were detected and CRYL1-IFT88 was successfully validated in the discovery sequencing sample and another 5 tumor samples with the recurrent rate of about 9.52% (6/63). The full length of CRYL1-IFT88 was obtained by 3′ and 5′ RACE. The function of the fusion transcript is closed to CRYL1 because it contained most of domain of CRYL1. According to the bioinformatics analysis, IFT88, reported as a tumor suppressor, might be seriously depressed in the tumor cell with this fusion because the transcript structure of IFT88 was totally changed. The function depression of IFT88 caused by gene fusion CRYL1-IFT88 might be associated with tumorigenesis or development of HCC.
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