LINC00265 maintains hepatocyte proliferation during liver regeneration by targeting miRNA-28-5p
Autor: | Hang Sun, Zhonglin Cui, Sheng Yu, Jie Zhou, Kai Wang, Qingping Li, Zhigang Hu |
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Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Apoptosis Applied Microbiology and Biotechnology Biochemistry Cell Line Analytical Chemistry 03 medical and health sciences 0302 clinical medicine Proliferating Cell Nuclear Antigen microRNA medicine Humans Molecular Biology Cell Proliferation Gene knockdown Chemistry Cell growth Regeneration (biology) Organic Chemistry General Medicine Cell cycle Liver regeneration Liver Regeneration Cell biology MicroRNAs Ki-67 Antigen 030104 developmental biology medicine.anatomical_structure Gene Knockdown Techniques 030220 oncology & carcinogenesis Hepatocyte Hepatocytes RNA Long Noncoding Biotechnology |
Zdroj: | Bioscience, Biotechnology, and Biochemistry. 85:528-536 |
ISSN: | 1347-6947 |
Popis: | Long noncoding RNAs have been implicated in many biological processes, but their roles in liver regeneration still need to be illustrated. Therefore, we aimed to investigate the role of LINC00265 as a pivotal regulator of hepatocyte proliferation during liver regeneration. It was found that LINC00265 is significantly upregulated in rat liver tissues at various time points after 2/3 liver resection. LINC00265 knockdown inhibited hepatocyte proliferation, induced cell apoptosis and led to G2/M phase cell cycle arrestment. In rats subjected to surgery, LINC00265 knockdown decreased liver/body weight ratio, attenuated improvement from liver damage and reduced Ki67 and PCNA expression. Luciferase reporter assays confirmed that miR-28-5p was a direct target of LINC00265, and inhibition of miR-28-5p abolished the effect of LINC00265 knockdown. In summary, LINC00265 might maintain hepatocyte proliferation by targeting miR-28-5p during liver regeneration and should be considered as a promising therapeutic option for hepatocyte regeneration after liver resection. |
Databáze: | OpenAIRE |
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