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氟苯达唑抑制A549、H460细胞增殖并促进自噬

BACKGROUND AND OBJECTIVE: Flubendazole is an anthelmintic and categorized in benzimidazole. Previous evidence indicates its suppression on proliferation of colon cancer and breast cancer cells. Our study aims to explore the effects of flubendazole on non-small cell lung cancer A549 and H460 cell lin...

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Formato: Online Artículo Texto
Lenguaje:English
Publicado: 中国肺癌杂志编辑部 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7260388/
https://www.ncbi.nlm.nih.gov/pubmed/32429634
http://dx.doi.org/10.3779/j.issn.1009-3419.2020.104.17
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collection PubMed
description BACKGROUND AND OBJECTIVE: Flubendazole is an anthelmintic and categorized in benzimidazole. Previous evidence indicates its suppression on proliferation of colon cancer and breast cancer cells. Our study aims to explore the effects of flubendazole on non-small cell lung cancer A549 and H460 cell lines and the underlying mechanism. METHODS: CCK-8 assay was used to detect the effect of flubendazole at different concentrations on viability of both cell lines A549 and H460. We used western blot to detect the expression levels of autophagy-related proteins p62 and LC3 after flubendazole treatment. Cells were transfected with tandem fluorescent adenovirus (mRFP-GFP-LC3), and the impact of flubendazole treatment on autophagic flux were analyzed. RESULTS: Cell viability analysis showed a dose-dependent inhibitory effect on proliferation of both A549 and H460, comparing to cells without flubendazole treating (P < 0.001). Level of p62 decreased and LC3 II/I ratio increased in cells treated with 2 μmol/L flubendazole for 24 h and 48 h, compared to control groups (P < 0.005). Red fluorescence signals increased in mRFP-GFP-LC3 transfected cells after flubendazole treating, suggesting an elevation in autophagic flux. CONCLUSION: Flubendazole may inhibit the proliferation of A549 and H460 cells and promote autophagy.
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spelling pubmed-72603882020-06-08 氟苯达唑抑制A549、H460细胞增殖并促进自噬 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: Flubendazole is an anthelmintic and categorized in benzimidazole. Previous evidence indicates its suppression on proliferation of colon cancer and breast cancer cells. Our study aims to explore the effects of flubendazole on non-small cell lung cancer A549 and H460 cell lines and the underlying mechanism. METHODS: CCK-8 assay was used to detect the effect of flubendazole at different concentrations on viability of both cell lines A549 and H460. We used western blot to detect the expression levels of autophagy-related proteins p62 and LC3 after flubendazole treatment. Cells were transfected with tandem fluorescent adenovirus (mRFP-GFP-LC3), and the impact of flubendazole treatment on autophagic flux were analyzed. RESULTS: Cell viability analysis showed a dose-dependent inhibitory effect on proliferation of both A549 and H460, comparing to cells without flubendazole treating (P < 0.001). Level of p62 decreased and LC3 II/I ratio increased in cells treated with 2 μmol/L flubendazole for 24 h and 48 h, compared to control groups (P < 0.005). Red fluorescence signals increased in mRFP-GFP-LC3 transfected cells after flubendazole treating, suggesting an elevation in autophagic flux. CONCLUSION: Flubendazole may inhibit the proliferation of A549 and H460 cells and promote autophagy. 中国肺癌杂志编辑部 2020-05-20 /pmc/articles/PMC7260388/ /pubmed/32429634 http://dx.doi.org/10.3779/j.issn.1009-3419.2020.104.17 Text en 版权所有©《中国肺癌杂志》编辑部2020 This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/.
spellingShingle 基础研究
氟苯达唑抑制A549、H460细胞增殖并促进自噬
title 氟苯达唑抑制A549、H460细胞增殖并促进自噬
title_full 氟苯达唑抑制A549、H460细胞增殖并促进自噬
title_fullStr 氟苯达唑抑制A549、H460细胞增殖并促进自噬
title_full_unstemmed 氟苯达唑抑制A549、H460细胞增殖并促进自噬
title_short 氟苯达唑抑制A549、H460细胞增殖并促进自噬
title_sort 氟苯达唑抑制a549、h460细胞增殖并促进自噬
topic 基础研究
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7260388/
https://www.ncbi.nlm.nih.gov/pubmed/32429634
http://dx.doi.org/10.3779/j.issn.1009-3419.2020.104.17
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