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A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway
The incidence and mortality rate of urological cancers is increasing yearly. Niclosamide has been repurposed as an anti‐cancer drug in recent years. Synthesized derivative of niclosamide was testified for its anti‐cancer activity in urological cancers. MTT assay was used to measure the cytotoxicity...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6089145/ https://www.ncbi.nlm.nih.gov/pubmed/29953738 http://dx.doi.org/10.1002/cam4.1635 |
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author | Wu, Chia‐Lun Chen, Chun‐Liang Huang, Hsu‐Shan Yu, Dah‐Shyong |
author_facet | Wu, Chia‐Lun Chen, Chun‐Liang Huang, Hsu‐Shan Yu, Dah‐Shyong |
author_sort | Wu, Chia‐Lun |
collection | PubMed |
description | The incidence and mortality rate of urological cancers is increasing yearly. Niclosamide has been repurposed as an anti‐cancer drug in recent years. Synthesized derivative of niclosamide was testified for its anti‐cancer activity in urological cancers. MTT assay was used to measure the cytotoxicity effect of niclosamide and its derivatives in urological cancer cell lines. Migratory ability was monitored by scratch migration assay. Apoptosis and cell cycle changes were analyzed by annexin V and PI staining. The apoptosis‐related signal proteins were evaluated by western blotting. T24 had the best drug sensitivity with the lowest IC (50) in niclosamide and B17 treatment than DU145 and Caki‐1 cells. After niclosamide and B17 treatment, the mitotic cells were decreased, but apoptotic bodies and morphology changes were not prominent in T24, Caki‐1, and DU145 cells. The migratory ability was inhibited in niclosamide treatment than control group on Caki‐1 cells and niclosamide and B17 treatment than control group on DU145 cells. Early apoptosis cells were increased after niclosamide and B17 treatment than control group without cell cycle changes in T24, Caki‐1, and DU145 cells. Programmed cell death was activated majorly through PAPR and bcl‐2 in T24 and caspase‐3 in Caki‐1 cells, respectively. Niclosamide and B17 derivative had good ability in inhibition proliferation and migratory ability in T24, Caki‐1, and DU145 cells without prominent morphology and apoptotic body changes. UCC cells are more sensitive to niclosamide and B17 treatment. Early apoptosis was induced after niclosamide and B17 treatment through different mechanisms in T24, Caki‐1, and DU145 cells. |
format | Online Article Text |
id | pubmed-6089145 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-60891452018-08-17 A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway Wu, Chia‐Lun Chen, Chun‐Liang Huang, Hsu‐Shan Yu, Dah‐Shyong Cancer Med Cancer Biology The incidence and mortality rate of urological cancers is increasing yearly. Niclosamide has been repurposed as an anti‐cancer drug in recent years. Synthesized derivative of niclosamide was testified for its anti‐cancer activity in urological cancers. MTT assay was used to measure the cytotoxicity effect of niclosamide and its derivatives in urological cancer cell lines. Migratory ability was monitored by scratch migration assay. Apoptosis and cell cycle changes were analyzed by annexin V and PI staining. The apoptosis‐related signal proteins were evaluated by western blotting. T24 had the best drug sensitivity with the lowest IC (50) in niclosamide and B17 treatment than DU145 and Caki‐1 cells. After niclosamide and B17 treatment, the mitotic cells were decreased, but apoptotic bodies and morphology changes were not prominent in T24, Caki‐1, and DU145 cells. The migratory ability was inhibited in niclosamide treatment than control group on Caki‐1 cells and niclosamide and B17 treatment than control group on DU145 cells. Early apoptosis cells were increased after niclosamide and B17 treatment than control group without cell cycle changes in T24, Caki‐1, and DU145 cells. Programmed cell death was activated majorly through PAPR and bcl‐2 in T24 and caspase‐3 in Caki‐1 cells, respectively. Niclosamide and B17 derivative had good ability in inhibition proliferation and migratory ability in T24, Caki‐1, and DU145 cells without prominent morphology and apoptotic body changes. UCC cells are more sensitive to niclosamide and B17 treatment. Early apoptosis was induced after niclosamide and B17 treatment through different mechanisms in T24, Caki‐1, and DU145 cells. John Wiley and Sons Inc. 2018-06-28 /pmc/articles/PMC6089145/ /pubmed/29953738 http://dx.doi.org/10.1002/cam4.1635 Text en © 2018 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Cancer Biology Wu, Chia‐Lun Chen, Chun‐Liang Huang, Hsu‐Shan Yu, Dah‐Shyong A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway |
title | A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway |
title_full | A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway |
title_fullStr | A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway |
title_full_unstemmed | A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway |
title_short | A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway |
title_sort | new niclosamide derivatives‐b17 can inhibit urological cancers growth through apoptosis‐related pathway |
topic | Cancer Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6089145/ https://www.ncbi.nlm.nih.gov/pubmed/29953738 http://dx.doi.org/10.1002/cam4.1635 |
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