Nitazoxanide inhibits osteosarcoma cells growth and metastasis by suppressing AKT/mTOR and Wnt/β-catenin signaling pathways

Osteosarcoma (OS) is the most prevalent malignant bone tumor with poor prognosis. Developing new drugs for the chemotherapy of OS has been a focal point and a major obstacle of OS treatment. Nitazoxanide (NTZ), a conventional anti-parasitic agent, has got increasingly noticed because of its favorabl...

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Published inBiological chemistry Vol. 403; no. 10; pp. 929 - 943
Main Authors Ye, Caihong, Wei, Mengqi, Huang, Huakun, Wang, Yuping, Zhang, Lulu, Yang, Chunmei, Huang, Yanran, Luo, Jinyong
Format Journal Article
LanguageEnglish
Published Berlin De Gruyter 27.09.2022
Walter de Gruyter GmbH
Subjects
AKT protein
Antiparasitic agents
Apoptosis
Bone cancer
Bone tumors
Cell cycle
Cell migration
Chemotherapy
G1 phase
Metastases
Metastasis
Osteosarcoma
Osteosarcoma cells
proliferation
Signal transduction
Signaling
signaling pathways
TOR protein
Wnt protein
β-Catenin
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Abstract Osteosarcoma (OS) is the most prevalent malignant bone tumor with poor prognosis. Developing new drugs for the chemotherapy of OS has been a focal point and a major obstacle of OS treatment. Nitazoxanide (NTZ), a conventional anti-parasitic agent, has got increasingly noticed because of its favorable antitumor potential. Herein, we investigated the effect of NTZ on human OS cells and . The results obtained showed that NTZ inhibited the proliferation, migration and invasion, arrested cell cycle at G1 phase, while induced apoptosis of OS cells. Mechanistically, NTZ suppressed the activity of AKT/mTOR and Wnt/β-catenin signaling pathways of OS cells. Consistent with the results , orthotopic implantation model of 143B OS cells further confirmed that NTZ inhibited OS cells growth and lung metastasis . Notably, NTZ caused no apparent damage to normal cells/tissues. In conclusion, NTZ may inhibit tumor growth and metastasis of human OS cells through suppressing AKT/mTOR and Wnt/β-catenin signaling pathways.
AbstractList Osteosarcoma (OS) is the most prevalent malignant bone tumor with poor prognosis. Developing new drugs for the chemotherapy of OS has been a focal point and a major obstacle of OS treatment. Nitazoxanide (NTZ), a conventional anti-parasitic agent, has got increasingly noticed because of its favorable antitumor potential. Herein, we investigated the effect of NTZ on human OS cells and . The results obtained showed that NTZ inhibited the proliferation, migration and invasion, arrested cell cycle at G1 phase, while induced apoptosis of OS cells. Mechanistically, NTZ suppressed the activity of AKT/mTOR and Wnt/β-catenin signaling pathways of OS cells. Consistent with the results , orthotopic implantation model of 143B OS cells further confirmed that NTZ inhibited OS cells growth and lung metastasis . Notably, NTZ caused no apparent damage to normal cells/tissues. In conclusion, NTZ may inhibit tumor growth and metastasis of human OS cells through suppressing AKT/mTOR and Wnt/β-catenin signaling pathways.
Osteosarcoma (OS) is the most prevalent malignant bone tumor with poor prognosis. Developing new drugs for the chemotherapy of OS has been a focal point and a major obstacle of OS treatment. Nitazoxanide (NTZ), a conventional anti-parasitic agent, has got increasingly noticed because of its favorable antitumor potential. Herein, we investigated the effect of NTZ on human OS cells in vitro and in vivo . The results obtained in vitro showed that NTZ inhibited the proliferation, migration and invasion, arrested cell cycle at G1 phase, while induced apoptosis of OS cells. Mechanistically, NTZ suppressed the activity of AKT/mTOR and Wnt/β-catenin signaling pathways of OS cells. Consistent with the results in vitro , orthotopic implantation model of 143B OS cells further confirmed that NTZ inhibited OS cells growth and lung metastasis in vivo . Notably, NTZ caused no apparent damage to normal cells/tissues. In conclusion, NTZ may inhibit tumor growth and metastasis of human OS cells through suppressing AKT/mTOR and Wnt/β-catenin signaling pathways.
Osteosarcoma (OS) is the most prevalent malignant bone tumor with poor prognosis. Developing new drugs for the chemotherapy of OS has been a focal point and a major obstacle of OS treatment. Nitazoxanide (NTZ), a conventional anti-parasitic agent, has got increasingly noticed because of its favorable antitumor potential. Herein, we investigated the effect of NTZ on human OS cells in vitro and in vivo. The results obtained in vitro showed that NTZ inhibited the proliferation, migration and invasion, arrested cell cycle at G1 phase, while induced apoptosis of OS cells. Mechanistically, NTZ suppressed the activity of AKT/mTOR and Wnt/β-catenin signaling pathways of OS cells. Consistent with the results in vitro, orthotopic implantation model of 143B OS cells further confirmed that NTZ inhibited OS cells growth and lung metastasis in vivo. Notably, NTZ caused no apparent damage to normal cells/tissues. In conclusion, NTZ may inhibit tumor growth and metastasis of human OS cells through suppressing AKT/mTOR and Wnt/β-catenin signaling pathways.
Osteosarcoma (OS) is the most prevalent malignant bone tumor with poor prognosis. Developing new drugs for the chemotherapy of OS has been a focal point and a major obstacle of OS treatment. Nitazoxanide (NTZ), a conventional anti-parasitic agent, has got increasingly noticed because of its favorable antitumor potential. Herein, we investigated the effect of NTZ on human OS cells in vitro and in vivo. The results obtained in vitro showed that NTZ inhibited the proliferation, migration and invasion, arrested cell cycle at G1 phase, while induced apoptosis of OS cells. Mechanistically, NTZ suppressed the activity of AKT/mTOR and Wnt/β-catenin signaling pathways of OS cells. Consistent with the results in vitro, orthotopic implantation model of 143B OS cells further confirmed that NTZ inhibited OS cells growth and lung metastasis in vivo. Notably, NTZ caused no apparent damage to normal cells/tissues. In conclusion, NTZ may inhibit tumor growth and metastasis of human OS cells through suppressing AKT/mTOR and Wnt/β-catenin signaling pathways.Osteosarcoma (OS) is the most prevalent malignant bone tumor with poor prognosis. Developing new drugs for the chemotherapy of OS has been a focal point and a major obstacle of OS treatment. Nitazoxanide (NTZ), a conventional anti-parasitic agent, has got increasingly noticed because of its favorable antitumor potential. Herein, we investigated the effect of NTZ on human OS cells in vitro and in vivo. The results obtained in vitro showed that NTZ inhibited the proliferation, migration and invasion, arrested cell cycle at G1 phase, while induced apoptosis of OS cells. Mechanistically, NTZ suppressed the activity of AKT/mTOR and Wnt/β-catenin signaling pathways of OS cells. Consistent with the results in vitro, orthotopic implantation model of 143B OS cells further confirmed that NTZ inhibited OS cells growth and lung metastasis in vivo. Notably, NTZ caused no apparent damage to normal cells/tissues. In conclusion, NTZ may inhibit tumor growth and metastasis of human OS cells through suppressing AKT/mTOR and Wnt/β-catenin signaling pathways.
Author Luo, Jinyong
Huang, Yanran
Wang, Yuping
Zhang, Lulu
Yang, Chunmei
Huang, Huakun
Ye, Caihong
Wei, Mengqi
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Cites_doi 10.1186/s13046-019-1274-0
10.3390/ijms22136923
10.1016/j.bbamcr.2020.118688
10.1080/17460441.2016.1216967
10.1038/s41419-018-1058-z
10.2174/1381612822666160512151028
10.3390/cancers13246226
10.1038/nature21034
10.1038/35000025
10.1177/1758835920940939
10.2174/1381612826666200131100630
10.1093/nar/gkw937
10.1093/nar/gkz382
10.1242/dev.091744
10.1038/309374a0
10.3892/or.2016.4922
10.1186/s12943-017-0700-1
10.1186/s12935-021-02411-y
10.1074/jbc.274.33.22932
10.1159/000066755
10.1016/j.tibs.2009.10.002
10.1093/nar/gky868
10.1016/j.mrfmmm.2014.05.005
10.18632/aging.203261
10.1358/dot.2021.57.7.3235211
10.1093/nar/gkx374
10.1080/14737140.2018.1413939
10.3390/cells10010172
10.1016/j.bjorl.2019.10.009
10.3390/cells10123435
10.21873/anticanres.14456
10.1002/fsn3.2636
10.1158/1535-7163.MCT-14-0792
10.1038/cdd.2017.186
10.1016/j.ccell.2021.03.010
10.1242/jcs.258966
10.1016/j.ejca.2017.09.036
10.7314/APJCP.2013.14.4.2201
10.1093/nar/gkaa1100
10.3892/or.2020.7817
10.1016/S0092-8674(00)81683-9
10.1186/1479-7364-5-6-709
10.1016/j.matbio.2015.06.003
10.1155/2012/704872
10.3390/cells9040976
10.1371/journal.pone.0095219
10.1080/14737140.2020.1760848
10.1038/nrc.2017.118
10.1158/1535-7163.MCT-12-1243
10.3390/ph14030230
10.1021/acsami.5b09112
10.1016/j.antiviral.2014.07.014
10.1016/j.bcp.2021.114588
10.1038/s41568-021-00332-6
10.3390/cells10123465
10.1159/000511765
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References 2023033110120831948_j_hsz-2022-0148_ref_036
2023033110120831948_j_hsz-2022-0148_ref_035
2023033110120831948_j_hsz-2022-0148_ref_038
2023033110120831948_j_hsz-2022-0148_ref_037
2023033110120831948_j_hsz-2022-0148_ref_039
2023033110120831948_j_hsz-2022-0148_ref_041
2023033110120831948_j_hsz-2022-0148_ref_040
2023033110120831948_j_hsz-2022-0148_ref_043
2023033110120831948_j_hsz-2022-0148_ref_042
2023033110120831948_j_hsz-2022-0148_ref_001
2023033110120831948_j_hsz-2022-0148_ref_045
2023033110120831948_j_hsz-2022-0148_ref_044
2023033110120831948_j_hsz-2022-0148_ref_003
2023033110120831948_j_hsz-2022-0148_ref_047
2023033110120831948_j_hsz-2022-0148_ref_002
2023033110120831948_j_hsz-2022-0148_ref_046
2023033110120831948_j_hsz-2022-0148_ref_005
2023033110120831948_j_hsz-2022-0148_ref_049
2023033110120831948_j_hsz-2022-0148_ref_004
2023033110120831948_j_hsz-2022-0148_ref_048
2023033110120831948_j_hsz-2022-0148_ref_007
2023033110120831948_j_hsz-2022-0148_ref_006
2023033110120831948_j_hsz-2022-0148_ref_009
2023033110120831948_j_hsz-2022-0148_ref_008
2023033110120831948_j_hsz-2022-0148_ref_050
2023033110120831948_j_hsz-2022-0148_ref_052
2023033110120831948_j_hsz-2022-0148_ref_051
2023033110120831948_j_hsz-2022-0148_ref_010
2023033110120831948_j_hsz-2022-0148_ref_054
2023033110120831948_j_hsz-2022-0148_ref_053
2023033110120831948_j_hsz-2022-0148_ref_012
2023033110120831948_j_hsz-2022-0148_ref_056
2023033110120831948_j_hsz-2022-0148_ref_011
2023033110120831948_j_hsz-2022-0148_ref_055
2023033110120831948_j_hsz-2022-0148_ref_014
2023033110120831948_j_hsz-2022-0148_ref_013
2023033110120831948_j_hsz-2022-0148_ref_016
2023033110120831948_j_hsz-2022-0148_ref_015
2023033110120831948_j_hsz-2022-0148_ref_018
2023033110120831948_j_hsz-2022-0148_ref_017
2023033110120831948_j_hsz-2022-0148_ref_019
2023033110120831948_j_hsz-2022-0148_ref_021
2023033110120831948_j_hsz-2022-0148_ref_020
2023033110120831948_j_hsz-2022-0148_ref_023
2023033110120831948_j_hsz-2022-0148_ref_022
2023033110120831948_j_hsz-2022-0148_ref_025
2023033110120831948_j_hsz-2022-0148_ref_024
2023033110120831948_j_hsz-2022-0148_ref_027
2023033110120831948_j_hsz-2022-0148_ref_026
2023033110120831948_j_hsz-2022-0148_ref_029
2023033110120831948_j_hsz-2022-0148_ref_028
2023033110120831948_j_hsz-2022-0148_ref_030
2023033110120831948_j_hsz-2022-0148_ref_032
2023033110120831948_j_hsz-2022-0148_ref_031
2023033110120831948_j_hsz-2022-0148_ref_034
2023033110120831948_j_hsz-2022-0148_ref_033
References_xml – ident: 2023033110120831948_j_hsz-2022-0148_ref_024
  doi: 10.1186/s13046-019-1274-0
– ident: 2023033110120831948_j_hsz-2022-0148_ref_047
  doi: 10.3390/ijms22136923
– ident: 2023033110120831948_j_hsz-2022-0148_ref_005
  doi: 10.1016/j.bbamcr.2020.118688
– ident: 2023033110120831948_j_hsz-2022-0148_ref_025
  doi: 10.1080/17460441.2016.1216967
– ident: 2023033110120831948_j_hsz-2022-0148_ref_051
  doi: 10.1038/s41419-018-1058-z
– ident: 2023033110120831948_j_hsz-2022-0148_ref_009
  doi: 10.2174/1381612822666160512151028
– ident: 2023033110120831948_j_hsz-2022-0148_ref_038
  doi: 10.3390/cancers13246226
– ident: 2023033110120831948_j_hsz-2022-0148_ref_032
  doi: 10.1038/nature21034
– ident: 2023033110120831948_j_hsz-2022-0148_ref_008
  doi: 10.1038/35000025
– ident: 2023033110120831948_j_hsz-2022-0148_ref_014
  doi: 10.1177/1758835920940939
– ident: 2023033110120831948_j_hsz-2022-0148_ref_042
  doi: 10.2174/1381612826666200131100630
– ident: 2023033110120831948_j_hsz-2022-0148_ref_049
  doi: 10.1093/nar/gkw937
– ident: 2023033110120831948_j_hsz-2022-0148_ref_011
  doi: 10.1093/nar/gkz382
– ident: 2023033110120831948_j_hsz-2022-0148_ref_029
  doi: 10.1242/dev.091744
– ident: 2023033110120831948_j_hsz-2022-0148_ref_031
  doi: 10.1038/309374a0
– ident: 2023033110120831948_j_hsz-2022-0148_ref_021
  doi: 10.3892/or.2016.4922
– ident: 2023033110120831948_j_hsz-2022-0148_ref_054
  doi: 10.1186/s12943-017-0700-1
– ident: 2023033110120831948_j_hsz-2022-0148_ref_028
  doi: 10.1186/s12935-021-02411-y
– ident: 2023033110120831948_j_hsz-2022-0148_ref_006
  doi: 10.1074/jbc.274.33.22932
– ident: 2023033110120831948_j_hsz-2022-0148_ref_026
  doi: 10.1159/000066755
– ident: 2023033110120831948_j_hsz-2022-0148_ref_053
  doi: 10.1016/j.tibs.2009.10.002
– ident: 2023033110120831948_j_hsz-2022-0148_ref_012
  doi: 10.1093/nar/gky868
– ident: 2023033110120831948_j_hsz-2022-0148_ref_013
  doi: 10.1016/j.mrfmmm.2014.05.005
– ident: 2023033110120831948_j_hsz-2022-0148_ref_056
  doi: 10.18632/aging.203261
– ident: 2023033110120831948_j_hsz-2022-0148_ref_004
  doi: 10.1358/dot.2021.57.7.3235211
– ident: 2023033110120831948_j_hsz-2022-0148_ref_052
  doi: 10.1093/nar/gkx374
– ident: 2023033110120831948_j_hsz-2022-0148_ref_019
  doi: 10.1080/14737140.2018.1413939
– ident: 2023033110120831948_j_hsz-2022-0148_ref_043
  doi: 10.3390/cells10010172
– ident: 2023033110120831948_j_hsz-2022-0148_ref_044
  doi: 10.1016/j.bjorl.2019.10.009
– ident: 2023033110120831948_j_hsz-2022-0148_ref_035
  doi: 10.3390/cells10123435
– ident: 2023033110120831948_j_hsz-2022-0148_ref_055
  doi: 10.21873/anticanres.14456
– ident: 2023033110120831948_j_hsz-2022-0148_ref_022
  doi: 10.1002/fsn3.2636
– ident: 2023033110120831948_j_hsz-2022-0148_ref_041
  doi: 10.1158/1535-7163.MCT-14-0792
– ident: 2023033110120831948_j_hsz-2022-0148_ref_023
  doi: 10.1038/cdd.2017.186
– ident: 2023033110120831948_j_hsz-2022-0148_ref_048
  doi: 10.1016/j.ccell.2021.03.010
– ident: 2023033110120831948_j_hsz-2022-0148_ref_039
  doi: 10.1242/jcs.258966
– ident: 2023033110120831948_j_hsz-2022-0148_ref_017
  doi: 10.1016/j.ejca.2017.09.036
– ident: 2023033110120831948_j_hsz-2022-0148_ref_037
  doi: 10.7314/APJCP.2013.14.4.2201
– ident: 2023033110120831948_j_hsz-2022-0148_ref_050
  doi: 10.1093/nar/gkaa1100
– ident: 2023033110120831948_j_hsz-2022-0148_ref_020
  doi: 10.3892/or.2020.7817
– ident: 2023033110120831948_j_hsz-2022-0148_ref_018
  doi: 10.1016/S0092-8674(00)81683-9
– ident: 2023033110120831948_j_hsz-2022-0148_ref_045
  doi: 10.1186/1479-7364-5-6-709
– ident: 2023033110120831948_j_hsz-2022-0148_ref_034
  doi: 10.1016/j.matbio.2015.06.003
– ident: 2023033110120831948_j_hsz-2022-0148_ref_002
  doi: 10.1155/2012/704872
– ident: 2023033110120831948_j_hsz-2022-0148_ref_010
  doi: 10.3390/cells9040976
– ident: 2023033110120831948_j_hsz-2022-0148_ref_036
  doi: 10.1371/journal.pone.0095219
– ident: 2023033110120831948_j_hsz-2022-0148_ref_033
  doi: 10.1080/14737140.2020.1760848
– ident: 2023033110120831948_j_hsz-2022-0148_ref_007
  doi: 10.1038/nrc.2017.118
– ident: 2023033110120831948_j_hsz-2022-0148_ref_016
  doi: 10.1158/1535-7163.MCT-12-1243
– ident: 2023033110120831948_j_hsz-2022-0148_ref_015
  doi: 10.3390/ph14030230
– ident: 2023033110120831948_j_hsz-2022-0148_ref_030
  doi: 10.1021/acsami.5b09112
– ident: 2023033110120831948_j_hsz-2022-0148_ref_040
  doi: 10.1016/j.antiviral.2014.07.014
– ident: 2023033110120831948_j_hsz-2022-0148_ref_046
  doi: 10.1016/j.bcp.2021.114588
– ident: 2023033110120831948_j_hsz-2022-0148_ref_027
  doi: 10.1038/s41568-021-00332-6
– ident: 2023033110120831948_j_hsz-2022-0148_ref_001
  doi: 10.3390/cells10123465
– ident: 2023033110120831948_j_hsz-2022-0148_ref_003
  doi: 10.1159/000511765
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Snippet Osteosarcoma (OS) is the most prevalent malignant bone tumor with poor prognosis. Developing new drugs for the chemotherapy of OS has been a focal point and a...
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SubjectTerms AKT protein
Antiparasitic agents
Apoptosis
Bone cancer
Bone tumors
Cell cycle
Cell migration
Chemotherapy
G1 phase
Metastases
Metastasis
Osteosarcoma
Osteosarcoma cells
proliferation
Signal transduction
Signaling
signaling pathways
TOR protein
Wnt protein
β-Catenin
Title Nitazoxanide inhibits osteosarcoma cells growth and metastasis by suppressing AKT/mTOR and Wnt/β-catenin signaling pathways
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