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Sasa veitchii extract induces anticancer effects via inhibition of cyclin D1 expression in MCF-7 cells

Sasa veitchii and other Sasa species are traditional medicinal herbs belonging to a group of Japanese bamboos collectively called Kumazasa, and these species possess the potential for a wide variety of uses. The present study aimed to elucidate the anticancer mechanisms exerted by S. veitchii extrac...

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Autores principales: Ichimaru, Yoshimi, Kanaeda, Natsuki, Tominaga, Sarah, Suzui, Masumi, Maeda, Tohru, Fujii, Hirohisa, Nakao, Makoto, Yoshioka, Hiroki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nagoya University 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7548257/
https://www.ncbi.nlm.nih.gov/pubmed/33132435
http://dx.doi.org/10.18999/nagjms.82.3.509
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author Ichimaru, Yoshimi
Kanaeda, Natsuki
Tominaga, Sarah
Suzui, Masumi
Maeda, Tohru
Fujii, Hirohisa
Nakao, Makoto
Yoshioka, Hiroki
author_facet Ichimaru, Yoshimi
Kanaeda, Natsuki
Tominaga, Sarah
Suzui, Masumi
Maeda, Tohru
Fujii, Hirohisa
Nakao, Makoto
Yoshioka, Hiroki
author_sort Ichimaru, Yoshimi
collection PubMed
description Sasa veitchii and other Sasa species are traditional medicinal herbs belonging to a group of Japanese bamboos collectively called Kumazasa, and these species possess the potential for a wide variety of uses. The present study aimed to elucidate the anticancer mechanisms exerted by S. veitchii extract (SE) against a human breast cancer cell line, MCF-7 cells. Freeze-dried Sunchlon(®) was used as the SE, and cell proliferation activity was measured using the [(3)H]-thymidine incorporation assay. Induction of apoptosis was assessed via Annexin V and caspase-3 fluorescent staining, the induction of necrosis was measured via propidium iodide staining, and cell cycle-related protein expression was determined using western blotting. The IC(50) value of the SE was 7.7 μg/mL in MCF-7 cells. Although the primary active ingredient in Sunchlon(®) is sodium copper chlorophyllin (0.25%), the present results indicated that ingredients other than SCC exert anti-cancer activities (the IC(50) value of SCC was 715 μg/mL), and late apoptosis or necrosis was induced in an SE dose-dependent manner. The expression levels of cyclin D1 and Cdk6 were decreased after SE treatment, and there was no change in the Cdk1/2 expression levels. Additionally, the expression of the necrosis-related cell death indicators RIP1 and RIP3 was increased in response to high-dose SE treatments, and this was indicative of cells preparing for programmed cell death. SE induces cell death in MCF-7 cells via the inhibition of cyclin D1 expression at low concentrations, and this extract induces programmed necrosis (necroptosis) by potentiating RIP1/RIP3 expression.
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spelling pubmed-75482572020-10-30 Sasa veitchii extract induces anticancer effects via inhibition of cyclin D1 expression in MCF-7 cells Ichimaru, Yoshimi Kanaeda, Natsuki Tominaga, Sarah Suzui, Masumi Maeda, Tohru Fujii, Hirohisa Nakao, Makoto Yoshioka, Hiroki Nagoya J Med Sci Original Paper Sasa veitchii and other Sasa species are traditional medicinal herbs belonging to a group of Japanese bamboos collectively called Kumazasa, and these species possess the potential for a wide variety of uses. The present study aimed to elucidate the anticancer mechanisms exerted by S. veitchii extract (SE) against a human breast cancer cell line, MCF-7 cells. Freeze-dried Sunchlon(®) was used as the SE, and cell proliferation activity was measured using the [(3)H]-thymidine incorporation assay. Induction of apoptosis was assessed via Annexin V and caspase-3 fluorescent staining, the induction of necrosis was measured via propidium iodide staining, and cell cycle-related protein expression was determined using western blotting. The IC(50) value of the SE was 7.7 μg/mL in MCF-7 cells. Although the primary active ingredient in Sunchlon(®) is sodium copper chlorophyllin (0.25%), the present results indicated that ingredients other than SCC exert anti-cancer activities (the IC(50) value of SCC was 715 μg/mL), and late apoptosis or necrosis was induced in an SE dose-dependent manner. The expression levels of cyclin D1 and Cdk6 were decreased after SE treatment, and there was no change in the Cdk1/2 expression levels. Additionally, the expression of the necrosis-related cell death indicators RIP1 and RIP3 was increased in response to high-dose SE treatments, and this was indicative of cells preparing for programmed cell death. SE induces cell death in MCF-7 cells via the inhibition of cyclin D1 expression at low concentrations, and this extract induces programmed necrosis (necroptosis) by potentiating RIP1/RIP3 expression. Nagoya University 2020-08 /pmc/articles/PMC7548257/ /pubmed/33132435 http://dx.doi.org/10.18999/nagjms.82.3.509 Text en http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an Open Access article distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. To view the details of this license, please visit (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Paper
Ichimaru, Yoshimi
Kanaeda, Natsuki
Tominaga, Sarah
Suzui, Masumi
Maeda, Tohru
Fujii, Hirohisa
Nakao, Makoto
Yoshioka, Hiroki
Sasa veitchii extract induces anticancer effects via inhibition of cyclin D1 expression in MCF-7 cells
title Sasa veitchii extract induces anticancer effects via inhibition of cyclin D1 expression in MCF-7 cells
title_full Sasa veitchii extract induces anticancer effects via inhibition of cyclin D1 expression in MCF-7 cells
title_fullStr Sasa veitchii extract induces anticancer effects via inhibition of cyclin D1 expression in MCF-7 cells
title_full_unstemmed Sasa veitchii extract induces anticancer effects via inhibition of cyclin D1 expression in MCF-7 cells
title_short Sasa veitchii extract induces anticancer effects via inhibition of cyclin D1 expression in MCF-7 cells
title_sort sasa veitchii extract induces anticancer effects via inhibition of cyclin d1 expression in mcf-7 cells
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7548257/
https://www.ncbi.nlm.nih.gov/pubmed/33132435
http://dx.doi.org/10.18999/nagjms.82.3.509
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