iNOS Promotes the Development of Osteosarcoma via Wnt/β-Catenin Pathway

Inducible nitric oxide synthase (iNOS), accompanied with protumor and antitumor activity, has been studied in multiple cancers. However, the role of iNOS expression in osteosarcoma (OS) is far from being fully understood. In present work, iNOS levels were detected in OS tissues and cell lines. Colon...

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Main Authors: Wei Chu, Lirong Cao, Gui Daokun, Jiali Zhao
Format: Article
Language:English
Published: Hindawi Limited 2021-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2021/4549221
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spelling doaj-a8629ec68e1040acb4cb8c538ec607a92021-08-30T00:00:02ZengHindawi LimitedJournal of Immunology Research2314-71562021-01-01202110.1155/2021/4549221iNOS Promotes the Development of Osteosarcoma via Wnt/β-Catenin PathwayWei Chu0Lirong Cao1Gui Daokun2Jiali Zhao3Department of OrthopedicsTeaching and Research Division of Surgical MedicineDepartment of OrthopaedicsDepartment of OrthopaedicsInducible nitric oxide synthase (iNOS), accompanied with protumor and antitumor activity, has been studied in multiple cancers. However, the role of iNOS expression in osteosarcoma (OS) is far from being fully understood. In present work, iNOS levels were detected in OS tissues and cell lines. Colony formation assay, Transwell assay, and fow cytometer were used to assess proliferation, migration, invasion, and apoptosis abilities in vitro after iNOS inhibition. Western blotting determined the expressions of iNOS, MMP2, MMP9, C-MYC, Ki67, PCNA, and β-catenin. Mice transfected with OS cells were to evaluate tumor formation. IHC assay was to evaluate the expressions of iNOS and β-catenin in mice. The results showed that iNOS was upregulated in both OS tissues and cells compared with that in matched normal tissues or cells. And we found that proliferation, migration, and invasion numbers of OS cells were decreased, and apoptosis numbers of OS cells were increased after iNOS inhibition. MMP2, MMP9, C-MYC, Ki67, and PCNA levels were also reduced in OS cells treated with iNOS inhibition. Else, iNOS inhibition would suppress β-catenin expression in OS cells to regulate MMP2, MMP9, C-MYC, Ki67, and PCNA expressions. In addition, tumor formation, iNOS expression, and β-catenin expression were inhibited in mice transplanted with iNOS knockout OS cells. These results indicated that iNOS might be a potential therapeutic target for OS.http://dx.doi.org/10.1155/2021/4549221
collection DOAJ
language English
format Article
sources DOAJ
author Wei Chu
Lirong Cao
Gui Daokun
Jiali Zhao
spellingShingle Wei Chu
Lirong Cao
Gui Daokun
Jiali Zhao
iNOS Promotes the Development of Osteosarcoma via Wnt/β-Catenin Pathway
Journal of Immunology Research
author_facet Wei Chu
Lirong Cao
Gui Daokun
Jiali Zhao
author_sort Wei Chu
title iNOS Promotes the Development of Osteosarcoma via Wnt/β-Catenin Pathway
title_short iNOS Promotes the Development of Osteosarcoma via Wnt/β-Catenin Pathway
title_full iNOS Promotes the Development of Osteosarcoma via Wnt/β-Catenin Pathway
title_fullStr iNOS Promotes the Development of Osteosarcoma via Wnt/β-Catenin Pathway
title_full_unstemmed iNOS Promotes the Development of Osteosarcoma via Wnt/β-Catenin Pathway
title_sort inos promotes the development of osteosarcoma via wnt/β-catenin pathway
publisher Hindawi Limited
series Journal of Immunology Research
issn 2314-7156
publishDate 2021-01-01
description Inducible nitric oxide synthase (iNOS), accompanied with protumor and antitumor activity, has been studied in multiple cancers. However, the role of iNOS expression in osteosarcoma (OS) is far from being fully understood. In present work, iNOS levels were detected in OS tissues and cell lines. Colony formation assay, Transwell assay, and fow cytometer were used to assess proliferation, migration, invasion, and apoptosis abilities in vitro after iNOS inhibition. Western blotting determined the expressions of iNOS, MMP2, MMP9, C-MYC, Ki67, PCNA, and β-catenin. Mice transfected with OS cells were to evaluate tumor formation. IHC assay was to evaluate the expressions of iNOS and β-catenin in mice. The results showed that iNOS was upregulated in both OS tissues and cells compared with that in matched normal tissues or cells. And we found that proliferation, migration, and invasion numbers of OS cells were decreased, and apoptosis numbers of OS cells were increased after iNOS inhibition. MMP2, MMP9, C-MYC, Ki67, and PCNA levels were also reduced in OS cells treated with iNOS inhibition. Else, iNOS inhibition would suppress β-catenin expression in OS cells to regulate MMP2, MMP9, C-MYC, Ki67, and PCNA expressions. In addition, tumor formation, iNOS expression, and β-catenin expression were inhibited in mice transplanted with iNOS knockout OS cells. These results indicated that iNOS might be a potential therapeutic target for OS.
url http://dx.doi.org/10.1155/2021/4549221
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AT jializhao inospromotesthedevelopmentofosteosarcomaviawntbcateninpathway
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