한빛사논문
- 조회472
Hyunho Cha 1, Minwoo Kim 1, Narae Ahn 1, Seong Dong Jeong 2, Elizaveta Ignatova 3, Sung Wook Chi 3,4, Hyeon Ho Kim 2,5 and Jungwook Hwang 1,6,*
1Graduate School for Biomedical Science & Engineering, Hanyang University, Seoul, Korea.
2Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul, Korea.
3Department of Life Sciences, Korea University, Seoul, Korea.
4KU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul, Korea.
5Institute for Future Medicine, Samsung Medical Center, Seoul, Korea.
6Hanyang Institute of Bioscience and Biotechnology, Hanyang University, Seoul, Korea.
*Corresponding author: correspondence to Jungwook Hwang
Abstract
UPF1, a novel posttranscriptional regulator, regulates the abundance of transcripts, including long noncoding RNAs (lncRNAs), and thus plays an important role in cell homeostasis. In this study, we revealed that UPF1 regulates the abundance of hepatocellular carcinoma upregulated EZH2-associated lncRNA (lncRNA-HEIH) by binding the CG-rich motif, thereby regulating hepatocellular carcinoma (HCC) tumorigenesis. UPF1-bound lncRNA-HEIH was susceptible to degradation mediated by UPF1 phosphorylation via SMG1 and SMG5. According to analysis of RNA-seq and public data on patients with liver cancer, the expression of lncRNA-HEIH increased the levels of miR-194-5p targets and was inversely correlated with miR-194-5p expression in HCC patients. Furthermore, UPF1 depletion upregulated lncRNA-HEIH, which acts as a decoy of miR-194-5p that targets GNA13, thereby promoting GNA13 expression and HCC proliferation. The UPF1/lncRNA-HEIH/miR-194-5p/GNA13 regulatory axis is suggested to play a crucial role in cell progression and may be a suitable target for HCC therapy.
논문정보
- Research article
- 2024년 02월 (BRIC 등록일 2024-02-01)
- 국내 연구진
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