Comprehensive transcriptome profiling of BET inhibitor-treated HepG2 cellsopen access
- Authors
- Baek, Mina; Chai, Jin Choul; Choi, Hae In; Yoo, Eunyoung; Binas, Bert; Lee, Young Seek; Jung, Kyoung Hwa; Chai, Young Gyu
- Issue Date
- Apr-2022
- Publisher
- Public Library of Science
- Citation
- PLoS ONE, v.17, no.4 April, pp 1 - 21
- Pages
- 21
- Indexed
- SCIE
SCOPUS
- Journal Title
- PLoS ONE
- Volume
- 17
- Number
- 4 April
- Start Page
- 1
- End Page
- 21
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/113288
- DOI
- 10.1371/journal.pone.0266966
- ISSN
- 1932-6203
- Abstract
- Hepatocellular carcinoma (HCC) is the most common primary liver cancer and poor prognosis. Emerging evidence suggests that epigenetic alterations play a crucial role in HCC, suggesting epigenetic inhibition as a promising therapeutic approach. Indeed, the bromodomain and extra-terminal (BET) inhibitors inhibit the proliferation and invasion of various cancers but still lack a strong mechanistic rationale. Here, we identified the differentially expressed mRNAs (DEmRNAs) and lncRNAs (DElncRNAs) in human HCC cell line HepG2 treated with the BET inhibitors, JQ1, OTX015, or ABBV-075. We analyzed the correlation between DEmRNAs and DElncRNAs in common for the three inhibitors based on their expression profiles and performed functional annotation pathway enrichment analysis. Most of these shared DEmRNAs and DElncRNAs, including some novel transcripts, were downregulated, indicating decreased proliferation/adhesion and increased apoptosis/inflammation. Our study suggests that BET proteins play a crucial role in regulating cancer progression-related genes and provide a valuable resource for novel putative biomarkers and therapeutic targets in HCC. © 2022 Baek et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
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