PLEKHA8P1 Promotes Tumor Progression and Indicates Poor Prognosis of Liver Cancer
- Authors
- Lee, Jiyeon; Hwang, Ji-Hyun; Chun, Harim; Woo, Wonjin; Oh, Sekyung; Choi, Jungmin; Kim, Lark Kyun
- Issue Date
- 7월-2021
- Publisher
- MDPI
- Keywords
- 5-fluorouracil; PLEKHA8; chemoresistance; hepatocellular carcinoma; long non-coding RNA; pseudogene
- Citation
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.22, no.14
- Indexed
- SCIE
SCOPUS
- Journal Title
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
- Volume
- 22
- Number
- 14
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/137180
- DOI
- 10.3390/ijms22147614
- ISSN
- 1661-6596
- Abstract
- Hepatocellular carcinoma (HCC) records the second-lowest 5-year survival rate despite the avalanche of research into diagnosis and therapy. One of the major obstacles in treatment is chemoresistance to drugs such as 5-fluorouracil (5-FU), making identification and elucidation of chemoresistance regulators highly valuable. As the regulatory landscape grows to encompass non-coding genes such as long non-coding RNAs (lncRNAs), a relatively new class of lncRNA has emerged in the form of pseudogene-derived lncRNAs. Through bioinformatics analyses of the TCGA LIHC dataset, we have systematically identified pseudogenes of prognostic value. Initial experimental validation of selected pseudogene-derived lncRNA (PLEKHA8P1) and its parental gene (PLEKHA8), a well-studied transport protein in Golgi complex recently implicated as an oncogene in both colorectal and liver cancer, indicates that the pseudogene/parental gene pair promotes tumor progression and that their dysregulated expression levels affect 5-FU-induced chemoresistance in human HCC cell line FT3-7. Our study has thus confirmed cancer-related functions of PLEKHA8, and laid the groundwork for identification and validation of oncogenic pseudogene-derived lncRNA that shows potential as a novel therapeutic target in circumventing chemoresistance induced by 5-FU.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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