UPF1 Inhibits Hepatocellular Carcinoma Growth through DUSP1/p53 Signal Pathwayopen access
- Authors
- Lee, Suman; Hwang, Yukyung; Kim, Tae Hun; Jeong, Jaemin; Choi, Dongho; Hwang, Jungwook
- Issue Date
- Apr-2022
- Publisher
- MDPI
- Keywords
- UPF1; hepatocellular carcinoma; posttranscriptional regulation; DUSP1
- Citation
- BIOMEDICINES, v.10, no.4, pp.1 - 12
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOMEDICINES
- Volume
- 10
- Number
- 4
- Start Page
- 1
- End Page
- 12
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/138954
- DOI
- 10.3390/biomedicines10040793
- ISSN
- 2227-9059
- Abstract
- Human hepatocellular carcinoma (HCC) has a high mortality rate because of the dearth of effective treatments. Multiple studies have shown that overexpression of UPF1, a key nonsense-mediated mRNA decay (NMD) factor, reduces HCC growth through various cell signaling pathways. However, the mechanism by which UPF1 expression retards HCC proliferation through the regulation of RNA stability remains unclear. By employing various UPF1 variants and transcriptome analysis, we revealed that overexpression of UPF1 variants, not UPF1-mediated NMD, reduces HCC tumorigenesis. Additionally, UPF1 variant overexpression reduced tumorigenesis in xenografted mice. Transcriptome analysis indicated that the level of dual specificity phosphatase 1 (DUSP1) was increased by UPF1 variants via posttranscriptional regulation. The UPF1 overexpression-mediated increase of DUSP1 activated tumor suppressor signaling, ultimately inhibiting cell growth. In this study, we highlighted the function of UPF1 as a tumor suppressor in HCC growth.
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Collections - 서울 의생명공학전문대학원 > 서울 의생명과학과 > 1. Journal Articles
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