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Cell cycle perturbations and apoptosis induced by isohomohalichondrin B (IHB), a natural marine compound
Isohomohalichondrin B (IHB), a novel marine compound with anti-tumoral activity, extracted from the Lissodendorix sponge, inhibits GTP binding to tubulin, preventing microtubule assembly. Cell cycle perturbations and apoptosis induced by IHB were investigated on selected human cancer cell lines by u...
Autores principales: | , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
1999
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362206/ https://www.ncbi.nlm.nih.gov/pubmed/9888468 http://dx.doi.org/10.1038/sj.bjc.6690044 |
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author | Bergamaschi, D Ronzoni, S Taverna, S Faretta, M Feudis, P De Faircloth, G Jimeno, J Erba, E D'Incalci, M |
author_facet | Bergamaschi, D Ronzoni, S Taverna, S Faretta, M Feudis, P De Faircloth, G Jimeno, J Erba, E D'Incalci, M |
author_sort | Bergamaschi, D |
collection | PubMed |
description | Isohomohalichondrin B (IHB), a novel marine compound with anti-tumoral activity, extracted from the Lissodendorix sponge, inhibits GTP binding to tubulin, preventing microtubule assembly. Cell cycle perturbations and apoptosis induced by IHB were investigated on selected human cancer cell lines by using flow cytometric and biochemical techniques. Monoparameter flow cytometric analysis showed that 1 h IHB exposure caused a delayed progression through S-phase, a dramatic block in G(2)M phase of the cell cycle and the appearance of tetraploid cell population in LoVo, LoVo/DX, MOLT-4 and K562 cells. At 24 h after IHB exposure, the majority of cells blocked in G(2)M were in prophase as assessed by morphological analysis and by the fact that they expressed high levels of cyclin A/cdc2 and cyclin B1/cdc2. At 48 h, all cells were tetraploid as assessed by biparameter cyclin A/DNA and cyclin B1/DNA content analysis. Apoptotic death was detected in both leukaemic MOLT-4 and K562 cells, which express wild-type and mutated p53 respectively, when the cells were blocked in mitotic prophase. In conclusion, IHB is a novel potent anti-tumour drug that causes delayed S-phase progression, mitotic block, tetraploidy and apoptosis in cancer cell lines. © 1999 Cancer Research Campaign |
format | Text |
id | pubmed-2362206 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1999 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-23622062009-09-10 Cell cycle perturbations and apoptosis induced by isohomohalichondrin B (IHB), a natural marine compound Bergamaschi, D Ronzoni, S Taverna, S Faretta, M Feudis, P De Faircloth, G Jimeno, J Erba, E D'Incalci, M Br J Cancer Regular Article Isohomohalichondrin B (IHB), a novel marine compound with anti-tumoral activity, extracted from the Lissodendorix sponge, inhibits GTP binding to tubulin, preventing microtubule assembly. Cell cycle perturbations and apoptosis induced by IHB were investigated on selected human cancer cell lines by using flow cytometric and biochemical techniques. Monoparameter flow cytometric analysis showed that 1 h IHB exposure caused a delayed progression through S-phase, a dramatic block in G(2)M phase of the cell cycle and the appearance of tetraploid cell population in LoVo, LoVo/DX, MOLT-4 and K562 cells. At 24 h after IHB exposure, the majority of cells blocked in G(2)M were in prophase as assessed by morphological analysis and by the fact that they expressed high levels of cyclin A/cdc2 and cyclin B1/cdc2. At 48 h, all cells were tetraploid as assessed by biparameter cyclin A/DNA and cyclin B1/DNA content analysis. Apoptotic death was detected in both leukaemic MOLT-4 and K562 cells, which express wild-type and mutated p53 respectively, when the cells were blocked in mitotic prophase. In conclusion, IHB is a novel potent anti-tumour drug that causes delayed S-phase progression, mitotic block, tetraploidy and apoptosis in cancer cell lines. © 1999 Cancer Research Campaign Nature Publishing Group 1999-01 /pmc/articles/PMC2362206/ /pubmed/9888468 http://dx.doi.org/10.1038/sj.bjc.6690044 Text en Copyright © 1999 Cancer Research Campaign https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Regular Article Bergamaschi, D Ronzoni, S Taverna, S Faretta, M Feudis, P De Faircloth, G Jimeno, J Erba, E D'Incalci, M Cell cycle perturbations and apoptosis induced by isohomohalichondrin B (IHB), a natural marine compound |
title | Cell cycle perturbations and apoptosis induced by isohomohalichondrin B (IHB), a natural marine compound |
title_full | Cell cycle perturbations and apoptosis induced by isohomohalichondrin B (IHB), a natural marine compound |
title_fullStr | Cell cycle perturbations and apoptosis induced by isohomohalichondrin B (IHB), a natural marine compound |
title_full_unstemmed | Cell cycle perturbations and apoptosis induced by isohomohalichondrin B (IHB), a natural marine compound |
title_short | Cell cycle perturbations and apoptosis induced by isohomohalichondrin B (IHB), a natural marine compound |
title_sort | cell cycle perturbations and apoptosis induced by isohomohalichondrin b (ihb), a natural marine compound |
topic | Regular Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362206/ https://www.ncbi.nlm.nih.gov/pubmed/9888468 http://dx.doi.org/10.1038/sj.bjc.6690044 |
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