Inhibitory effects of diarsenic trioxide (As2O3) on hepatocellular carcinoma cells exerted by regulation of promyelocytic leukemia protein levels
Autor(a) principal: | |
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Data de Publicação: | 2023 |
Outros Autores: | , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Bioscience journal (Online) |
Texto Completo: | https://seer.ufu.br/index.php/biosciencejournal/article/view/63086 |
Resumo: | Previous Chinese research revealed that diarsenic trioxide (As2O3) inhibits acute promyelocytic leukemia (PML) cell proliferation and initiates apoptosis through degradation of the PML-retinoic acid receptor protein. This study was to analyse whether As2O3 also had an effect on hepatocellular carcinoma (HCC) cells. As2O3 effects on various HCC cell lines and primary HCC cells were investigated in time and dose series, including measurements of cell growth, PML mRNA and protein expression, xenografted tumor formation, and the self-renewal Oct4 and hepatocyte marker expressions in mouse model xenografts or cells treated with PML siRNA. The results were analyzed by immunocytochemistry, quantitative reverse transcription PCR and western blotting as well as indocyanine green and Periodic Acid Schiff staining. As2O3 inhibited HCC cell and HCC cell-derived xenograft tumor formation in a time-dependent manner and reduced PML protein expression in HCC cells, but had limited effects on PML mRNA levels in cell nuclei. The HCC cell line HuH7 treated with As2O3 showed a decreased expression of alpha-fetoprotein and increased expression and transcription of mature hepatocyte markers, indicating differentiation of HCC cells into hepatocytes. Cytokeratin 18 protein and mRNA levels as well as tyrosine aminotransferase and apolipoprotein B mRNA transcriptions were enhanced by As2O3 as were the numbers of indocyanine green and Periodic Acid Schiff stained cells. In addition, As2O3 downregulated the expression of Oct4. In conclusion, since As2O3 inhibited HCC cell proliferation and HCC cell-derived xenograft tumor formation it is suggested that an appropriate concentration of As2O3 might be a promising therapy to treat HCC. |
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Inhibitory effects of diarsenic trioxide (As2O3) on hepatocellular carcinoma cells exerted by regulation of promyelocytic leukemia protein levelsAs2O3Hepatocellular carcinomaPromyelocytic leukemia (PML). Transcription factor 4.Biological SciencesPrevious Chinese research revealed that diarsenic trioxide (As2O3) inhibits acute promyelocytic leukemia (PML) cell proliferation and initiates apoptosis through degradation of the PML-retinoic acid receptor protein. This study was to analyse whether As2O3 also had an effect on hepatocellular carcinoma (HCC) cells. As2O3 effects on various HCC cell lines and primary HCC cells were investigated in time and dose series, including measurements of cell growth, PML mRNA and protein expression, xenografted tumor formation, and the self-renewal Oct4 and hepatocyte marker expressions in mouse model xenografts or cells treated with PML siRNA. The results were analyzed by immunocytochemistry, quantitative reverse transcription PCR and western blotting as well as indocyanine green and Periodic Acid Schiff staining. As2O3 inhibited HCC cell and HCC cell-derived xenograft tumor formation in a time-dependent manner and reduced PML protein expression in HCC cells, but had limited effects on PML mRNA levels in cell nuclei. The HCC cell line HuH7 treated with As2O3 showed a decreased expression of alpha-fetoprotein and increased expression and transcription of mature hepatocyte markers, indicating differentiation of HCC cells into hepatocytes. Cytokeratin 18 protein and mRNA levels as well as tyrosine aminotransferase and apolipoprotein B mRNA transcriptions were enhanced by As2O3 as were the numbers of indocyanine green and Periodic Acid Schiff stained cells. In addition, As2O3 downregulated the expression of Oct4. In conclusion, since As2O3 inhibited HCC cell proliferation and HCC cell-derived xenograft tumor formation it is suggested that an appropriate concentration of As2O3 might be a promising therapy to treat HCC.Universidade Federal de Uberlândia2023-03-31info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://seer.ufu.br/index.php/biosciencejournal/article/view/6308610.14393/BJ-v39n0a2023-63086Bioscience Journal ; Vol. 39 (2023): Continuous Publication; e39052Bioscience Journal ; v. 39 (2023): Continuous Publication; e390521981-3163reponame:Bioscience journal (Online)instname:Universidade Federal de Uberlândia (UFU)instacron:UFUenghttps://seer.ufu.br/index.php/biosciencejournal/article/view/63086/35867China; Contemporary Copyright (c) 2023 Guowu Zhang, Wei Wang, Yukai Jin, Shilong Jin, Lei Mi, Xiaowen Song, He Li, Juan Liaohttps://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessZhang, GuowuWang, Wei Jin, YukaiJin, ShilongMi, LeiSong, XiaowenLi, HeLiao, Juan2024-01-31T19:16:18Zoai:ojs.www.seer.ufu.br:article/63086Revistahttps://seer.ufu.br/index.php/biosciencejournalPUBhttps://seer.ufu.br/index.php/biosciencejournal/oaibiosciencej@ufu.br||1981-31631516-3725opendoar:2024-01-31T19:16:18Bioscience journal (Online) - Universidade Federal de Uberlândia (UFU)false |
dc.title.none.fl_str_mv |
Inhibitory effects of diarsenic trioxide (As2O3) on hepatocellular carcinoma cells exerted by regulation of promyelocytic leukemia protein levels |
title |
Inhibitory effects of diarsenic trioxide (As2O3) on hepatocellular carcinoma cells exerted by regulation of promyelocytic leukemia protein levels |
spellingShingle |
Inhibitory effects of diarsenic trioxide (As2O3) on hepatocellular carcinoma cells exerted by regulation of promyelocytic leukemia protein levels Zhang, Guowu As2O3 Hepatocellular carcinoma Promyelocytic leukemia (PML). Transcription factor 4. Biological Sciences |
title_short |
Inhibitory effects of diarsenic trioxide (As2O3) on hepatocellular carcinoma cells exerted by regulation of promyelocytic leukemia protein levels |
title_full |
Inhibitory effects of diarsenic trioxide (As2O3) on hepatocellular carcinoma cells exerted by regulation of promyelocytic leukemia protein levels |
title_fullStr |
Inhibitory effects of diarsenic trioxide (As2O3) on hepatocellular carcinoma cells exerted by regulation of promyelocytic leukemia protein levels |
title_full_unstemmed |
Inhibitory effects of diarsenic trioxide (As2O3) on hepatocellular carcinoma cells exerted by regulation of promyelocytic leukemia protein levels |
title_sort |
Inhibitory effects of diarsenic trioxide (As2O3) on hepatocellular carcinoma cells exerted by regulation of promyelocytic leukemia protein levels |
author |
Zhang, Guowu |
author_facet |
Zhang, Guowu Wang, Wei Jin, Yukai Jin, Shilong Mi, Lei Song, Xiaowen Li, He Liao, Juan |
author_role |
author |
author2 |
Wang, Wei Jin, Yukai Jin, Shilong Mi, Lei Song, Xiaowen Li, He Liao, Juan |
author2_role |
author author author author author author author |
dc.contributor.author.fl_str_mv |
Zhang, Guowu Wang, Wei Jin, Yukai Jin, Shilong Mi, Lei Song, Xiaowen Li, He Liao, Juan |
dc.subject.por.fl_str_mv |
As2O3 Hepatocellular carcinoma Promyelocytic leukemia (PML). Transcription factor 4. Biological Sciences |
topic |
As2O3 Hepatocellular carcinoma Promyelocytic leukemia (PML). Transcription factor 4. Biological Sciences |
description |
Previous Chinese research revealed that diarsenic trioxide (As2O3) inhibits acute promyelocytic leukemia (PML) cell proliferation and initiates apoptosis through degradation of the PML-retinoic acid receptor protein. This study was to analyse whether As2O3 also had an effect on hepatocellular carcinoma (HCC) cells. As2O3 effects on various HCC cell lines and primary HCC cells were investigated in time and dose series, including measurements of cell growth, PML mRNA and protein expression, xenografted tumor formation, and the self-renewal Oct4 and hepatocyte marker expressions in mouse model xenografts or cells treated with PML siRNA. The results were analyzed by immunocytochemistry, quantitative reverse transcription PCR and western blotting as well as indocyanine green and Periodic Acid Schiff staining. As2O3 inhibited HCC cell and HCC cell-derived xenograft tumor formation in a time-dependent manner and reduced PML protein expression in HCC cells, but had limited effects on PML mRNA levels in cell nuclei. The HCC cell line HuH7 treated with As2O3 showed a decreased expression of alpha-fetoprotein and increased expression and transcription of mature hepatocyte markers, indicating differentiation of HCC cells into hepatocytes. Cytokeratin 18 protein and mRNA levels as well as tyrosine aminotransferase and apolipoprotein B mRNA transcriptions were enhanced by As2O3 as were the numbers of indocyanine green and Periodic Acid Schiff stained cells. In addition, As2O3 downregulated the expression of Oct4. In conclusion, since As2O3 inhibited HCC cell proliferation and HCC cell-derived xenograft tumor formation it is suggested that an appropriate concentration of As2O3 might be a promising therapy to treat HCC. |
publishDate |
2023 |
dc.date.none.fl_str_mv |
2023-03-31 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://seer.ufu.br/index.php/biosciencejournal/article/view/63086 10.14393/BJ-v39n0a2023-63086 |
url |
https://seer.ufu.br/index.php/biosciencejournal/article/view/63086 |
identifier_str_mv |
10.14393/BJ-v39n0a2023-63086 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
https://seer.ufu.br/index.php/biosciencejournal/article/view/63086/35867 |
dc.rights.driver.fl_str_mv |
https://creativecommons.org/licenses/by/4.0 info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by/4.0 |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.coverage.none.fl_str_mv |
China; Contemporary |
dc.publisher.none.fl_str_mv |
Universidade Federal de Uberlândia |
publisher.none.fl_str_mv |
Universidade Federal de Uberlândia |
dc.source.none.fl_str_mv |
Bioscience Journal ; Vol. 39 (2023): Continuous Publication; e39052 Bioscience Journal ; v. 39 (2023): Continuous Publication; e39052 1981-3163 reponame:Bioscience journal (Online) instname:Universidade Federal de Uberlândia (UFU) instacron:UFU |
instname_str |
Universidade Federal de Uberlândia (UFU) |
instacron_str |
UFU |
institution |
UFU |
reponame_str |
Bioscience journal (Online) |
collection |
Bioscience journal (Online) |
repository.name.fl_str_mv |
Bioscience journal (Online) - Universidade Federal de Uberlândia (UFU) |
repository.mail.fl_str_mv |
biosciencej@ufu.br|| |
_version_ |
1797069065188016128 |