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Pre-mRNA Processing Factor 8 Accelerates the Progression of Hepatocellular Carcinoma by Regulating the PI3K/Akt Pathway

BACKGROUND: The specific function of pre-mRNA processing factors (Prps) in human malignancies has not been yet investigated. The aim of the present study was to determine the impacts of Prp8 in a common human malignancy, hepatocellular carcinoma (HCC). MATERIALS AND METHODS: RT-qPCR and Western blot...

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Autores principales: Wang, Shouhan, Wang, Min, Wang, Bin, Chen, Jiaqi, Cheng, Xianbin, Sun, Xiaodan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7263830/
https://www.ncbi.nlm.nih.gov/pubmed/32547101
http://dx.doi.org/10.2147/OTT.S241214
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author Wang, Shouhan
Wang, Min
Wang, Bin
Chen, Jiaqi
Cheng, Xianbin
Sun, Xiaodan
author_facet Wang, Shouhan
Wang, Min
Wang, Bin
Chen, Jiaqi
Cheng, Xianbin
Sun, Xiaodan
author_sort Wang, Shouhan
collection PubMed
description BACKGROUND: The specific function of pre-mRNA processing factors (Prps) in human malignancies has not been yet investigated. The aim of the present study was to determine the impacts of Prp8 in a common human malignancy, hepatocellular carcinoma (HCC). MATERIALS AND METHODS: RT-qPCR and Western blotting were performed to measure the expression levels of Prp8 in various HCC cell lines and HCC tissues. A hepatic astrocyte line was transfected with a eukaryotic expression plasmid to overexpress Prp8. In addition, the endogenous expression level of Prp8 in HCC cells was silenced using a short hairpin RNA method, and the role of Prp8 on cell proliferation and migration was examined by Cell Counting Kit-8, wound healing assay and Transwell assays following knockdown in HCC cells, and overexpression in astrocytes. RESULTS: Upregulation of Prp8 expression was found to be associated with poor clinical outcomes in patients with HCC. The upregulation of Prp8 promoted cell viability, metastasis and the activity of the PI3K/Akt pathway in hepatic astrocytes cells and HCC cells. Interestingly, loss of Prp8 had no obvious impact on cell viability and migration in hepatic astrocytes, but significantly inhibit the cell malignancy of HCC cells. Functionally, the inhibition of the PI3K/Akt pathway reversed the increased cell viability and migration of HCC cells induced by Prp8 via inhibiting EMT process. CONCLUSION: Collectively, the present results suggested that Prp8 served as a tumor promoter in HCC by targeting and regulating the PI3K/Akt pathway.
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spelling pubmed-72638302020-06-15 Pre-mRNA Processing Factor 8 Accelerates the Progression of Hepatocellular Carcinoma by Regulating the PI3K/Akt Pathway Wang, Shouhan Wang, Min Wang, Bin Chen, Jiaqi Cheng, Xianbin Sun, Xiaodan Onco Targets Ther Original Research BACKGROUND: The specific function of pre-mRNA processing factors (Prps) in human malignancies has not been yet investigated. The aim of the present study was to determine the impacts of Prp8 in a common human malignancy, hepatocellular carcinoma (HCC). MATERIALS AND METHODS: RT-qPCR and Western blotting were performed to measure the expression levels of Prp8 in various HCC cell lines and HCC tissues. A hepatic astrocyte line was transfected with a eukaryotic expression plasmid to overexpress Prp8. In addition, the endogenous expression level of Prp8 in HCC cells was silenced using a short hairpin RNA method, and the role of Prp8 on cell proliferation and migration was examined by Cell Counting Kit-8, wound healing assay and Transwell assays following knockdown in HCC cells, and overexpression in astrocytes. RESULTS: Upregulation of Prp8 expression was found to be associated with poor clinical outcomes in patients with HCC. The upregulation of Prp8 promoted cell viability, metastasis and the activity of the PI3K/Akt pathway in hepatic astrocytes cells and HCC cells. Interestingly, loss of Prp8 had no obvious impact on cell viability and migration in hepatic astrocytes, but significantly inhibit the cell malignancy of HCC cells. Functionally, the inhibition of the PI3K/Akt pathway reversed the increased cell viability and migration of HCC cells induced by Prp8 via inhibiting EMT process. CONCLUSION: Collectively, the present results suggested that Prp8 served as a tumor promoter in HCC by targeting and regulating the PI3K/Akt pathway. Dove 2020-05-26 /pmc/articles/PMC7263830/ /pubmed/32547101 http://dx.doi.org/10.2147/OTT.S241214 Text en © 2020 Wang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Wang, Shouhan
Wang, Min
Wang, Bin
Chen, Jiaqi
Cheng, Xianbin
Sun, Xiaodan
Pre-mRNA Processing Factor 8 Accelerates the Progression of Hepatocellular Carcinoma by Regulating the PI3K/Akt Pathway
title Pre-mRNA Processing Factor 8 Accelerates the Progression of Hepatocellular Carcinoma by Regulating the PI3K/Akt Pathway
title_full Pre-mRNA Processing Factor 8 Accelerates the Progression of Hepatocellular Carcinoma by Regulating the PI3K/Akt Pathway
title_fullStr Pre-mRNA Processing Factor 8 Accelerates the Progression of Hepatocellular Carcinoma by Regulating the PI3K/Akt Pathway
title_full_unstemmed Pre-mRNA Processing Factor 8 Accelerates the Progression of Hepatocellular Carcinoma by Regulating the PI3K/Akt Pathway
title_short Pre-mRNA Processing Factor 8 Accelerates the Progression of Hepatocellular Carcinoma by Regulating the PI3K/Akt Pathway
title_sort pre-mrna processing factor 8 accelerates the progression of hepatocellular carcinoma by regulating the pi3k/akt pathway
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7263830/
https://www.ncbi.nlm.nih.gov/pubmed/32547101
http://dx.doi.org/10.2147/OTT.S241214
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