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Propofol Suppresses Cell Progression by Inhibiting CCL18 Expression in Hepatoblastoma
BACKGROUND: Propofol is an anesthetic commonly used clinically and has been found to have antitumor activity in various cancers. The purpose of this study was to investigate the role of propofol in hepatoblastoma (HB). METHODS: CCK-8 and transwell were used to measure cell proliferation, migration,...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8331318/ https://www.ncbi.nlm.nih.gov/pubmed/34354751 http://dx.doi.org/10.1155/2021/6880473 |
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author | Zhang, Hua Lin, Pingling Fu, Lei Li, Zhijun Ding, Yan |
author_facet | Zhang, Hua Lin, Pingling Fu, Lei Li, Zhijun Ding, Yan |
author_sort | Zhang, Hua |
collection | PubMed |
description | BACKGROUND: Propofol is an anesthetic commonly used clinically and has been found to have antitumor activity in various cancers. The purpose of this study was to investigate the role of propofol in hepatoblastoma (HB). METHODS: CCK-8 and transwell were used to measure cell proliferation, migration, and invasion in HB cells. Cell apoptosis rate was measured by FCM. The expression of CCL18 in HB tissues and cells was detected by RT-qPCR. Western blotting was used to explore the protein expression of CCK18- and PI3K/AKT-related proteins. RESULTS: The expression of CCL18 in HB tissues and cells was overexpressed compared with control groups. CCL18 knockdown was found to notably block cell proliferation and progression, while enhancing cell apoptosis in HuH-6 and HepT1 cells. Furthermore, propofol suppressed the proliferation of HB cells in a dose-dependent manner. According to the results, we chose 5 μg/mL of propofol-treated cells for 48 hours as the subsequent experimental conditions. We found that propofol (5 μg/mL, 48 h) significantly blocked cell migration and invasion, but induced cell apoptosis in HuH-6 and HepT1 cells. In addition, CCK18 overexpression facilitated cell progression in HB cells, while propofol dramatically suppressed the effect of CCK18. Besides that, propofol suppressed the PI3K/AKT pathway. CONCLUSION: Propofol suppressed the development of HB cells by inhibiting CCK18 expression and the PI3K/AKT pathway. Therefore, we infer that propofol plays a role in the treatment of HB. |
format | Online Article Text |
id | pubmed-8331318 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-83313182021-08-04 Propofol Suppresses Cell Progression by Inhibiting CCL18 Expression in Hepatoblastoma Zhang, Hua Lin, Pingling Fu, Lei Li, Zhijun Ding, Yan J Oncol Research Article BACKGROUND: Propofol is an anesthetic commonly used clinically and has been found to have antitumor activity in various cancers. The purpose of this study was to investigate the role of propofol in hepatoblastoma (HB). METHODS: CCK-8 and transwell were used to measure cell proliferation, migration, and invasion in HB cells. Cell apoptosis rate was measured by FCM. The expression of CCL18 in HB tissues and cells was detected by RT-qPCR. Western blotting was used to explore the protein expression of CCK18- and PI3K/AKT-related proteins. RESULTS: The expression of CCL18 in HB tissues and cells was overexpressed compared with control groups. CCL18 knockdown was found to notably block cell proliferation and progression, while enhancing cell apoptosis in HuH-6 and HepT1 cells. Furthermore, propofol suppressed the proliferation of HB cells in a dose-dependent manner. According to the results, we chose 5 μg/mL of propofol-treated cells for 48 hours as the subsequent experimental conditions. We found that propofol (5 μg/mL, 48 h) significantly blocked cell migration and invasion, but induced cell apoptosis in HuH-6 and HepT1 cells. In addition, CCK18 overexpression facilitated cell progression in HB cells, while propofol dramatically suppressed the effect of CCK18. Besides that, propofol suppressed the PI3K/AKT pathway. CONCLUSION: Propofol suppressed the development of HB cells by inhibiting CCK18 expression and the PI3K/AKT pathway. Therefore, we infer that propofol plays a role in the treatment of HB. Hindawi 2021-07-26 /pmc/articles/PMC8331318/ /pubmed/34354751 http://dx.doi.org/10.1155/2021/6880473 Text en Copyright © 2021 Hua Zhang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Zhang, Hua Lin, Pingling Fu, Lei Li, Zhijun Ding, Yan Propofol Suppresses Cell Progression by Inhibiting CCL18 Expression in Hepatoblastoma |
title | Propofol Suppresses Cell Progression by Inhibiting CCL18 Expression in Hepatoblastoma |
title_full | Propofol Suppresses Cell Progression by Inhibiting CCL18 Expression in Hepatoblastoma |
title_fullStr | Propofol Suppresses Cell Progression by Inhibiting CCL18 Expression in Hepatoblastoma |
title_full_unstemmed | Propofol Suppresses Cell Progression by Inhibiting CCL18 Expression in Hepatoblastoma |
title_short | Propofol Suppresses Cell Progression by Inhibiting CCL18 Expression in Hepatoblastoma |
title_sort | propofol suppresses cell progression by inhibiting ccl18 expression in hepatoblastoma |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8331318/ https://www.ncbi.nlm.nih.gov/pubmed/34354751 http://dx.doi.org/10.1155/2021/6880473 |
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