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The Effects and Mechanisms of Sennoside A on Inducing Cytotoxicity, Apoptosis, and Inhibiting Metastasis in Human Chondrosarcoma Cells

Currently, developing therapeutic strategies for chondrosarcoma (CS) remains important. Sennoside A (SA), a dianthrone glycoside from Senna and Rhubarb, is widely used as an irritant laxative, weight-loss agent, or dietary supplement, which possesses various bioactive properties such as laxative, an...

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Autores principales: Le, Jiamei, Ji, Houlin, Pi, Peixian, Chen, Kaijie, Gu, Xuefeng, Ma, Yujie, Fu, Yi, Sun, Yongning, Zhou, Xiaoxiao, Wu, Hailong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9451980/
https://www.ncbi.nlm.nih.gov/pubmed/36091590
http://dx.doi.org/10.1155/2022/8063497
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author Le, Jiamei
Ji, Houlin
Pi, Peixian
Chen, Kaijie
Gu, Xuefeng
Ma, Yujie
Fu, Yi
Sun, Yongning
Zhou, Xiaoxiao
Wu, Hailong
author_facet Le, Jiamei
Ji, Houlin
Pi, Peixian
Chen, Kaijie
Gu, Xuefeng
Ma, Yujie
Fu, Yi
Sun, Yongning
Zhou, Xiaoxiao
Wu, Hailong
author_sort Le, Jiamei
collection PubMed
description Currently, developing therapeutic strategies for chondrosarcoma (CS) remains important. Sennoside A (SA), a dianthrone glycoside from Senna and Rhubarb, is widely used as an irritant laxative, weight-loss agent, or dietary supplement, which possesses various bioactive properties such as laxative, antiobesity, and hypoglycemic activities. For the first time, our results suggested that cell proliferation and metastasis were inhibited by SA in CS SW1353 cells. SA induced cell growth arrest by inhibiting cell proliferation. The changes of N-cadherin and E-cadherin levels, the markers associated with epithelial mesenchymal transition (EMT), suggested the EMT-related mechanism of SA in inhibiting cell metastasis. Besides, SA significantly stimulated apoptosis in CS SW1353 cells, leading to cell death. The increase of Bax/Bcl2 ratio confirmed that the internal mitochondrial pathway of apoptosis was regulated by SA. In addition, the prediction of network pharmacology analysis suggested that the possible pathways of SA treatment for CS included the Wnt signaling pathway. Notably, the protein levels of the components in the Wnt pathway, such as Wnt3a, β-catenin, and c-Myc, were downregulated by SA in CS SW1353 cells. To sum up, these results demonstrated that the suppression of the growth, metastasis and the stimulation of cytotoxicity, and apoptosis mediated by SA in CS SW1353 cells were possibly caused by the inhibition of the Wnt/β-catenin pathway, indicating an underlying therapeutic prospect of SA for chondrosarcoma.
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spelling pubmed-94519802022-09-08 The Effects and Mechanisms of Sennoside A on Inducing Cytotoxicity, Apoptosis, and Inhibiting Metastasis in Human Chondrosarcoma Cells Le, Jiamei Ji, Houlin Pi, Peixian Chen, Kaijie Gu, Xuefeng Ma, Yujie Fu, Yi Sun, Yongning Zhou, Xiaoxiao Wu, Hailong Evid Based Complement Alternat Med Research Article Currently, developing therapeutic strategies for chondrosarcoma (CS) remains important. Sennoside A (SA), a dianthrone glycoside from Senna and Rhubarb, is widely used as an irritant laxative, weight-loss agent, or dietary supplement, which possesses various bioactive properties such as laxative, antiobesity, and hypoglycemic activities. For the first time, our results suggested that cell proliferation and metastasis were inhibited by SA in CS SW1353 cells. SA induced cell growth arrest by inhibiting cell proliferation. The changes of N-cadherin and E-cadherin levels, the markers associated with epithelial mesenchymal transition (EMT), suggested the EMT-related mechanism of SA in inhibiting cell metastasis. Besides, SA significantly stimulated apoptosis in CS SW1353 cells, leading to cell death. The increase of Bax/Bcl2 ratio confirmed that the internal mitochondrial pathway of apoptosis was regulated by SA. In addition, the prediction of network pharmacology analysis suggested that the possible pathways of SA treatment for CS included the Wnt signaling pathway. Notably, the protein levels of the components in the Wnt pathway, such as Wnt3a, β-catenin, and c-Myc, were downregulated by SA in CS SW1353 cells. To sum up, these results demonstrated that the suppression of the growth, metastasis and the stimulation of cytotoxicity, and apoptosis mediated by SA in CS SW1353 cells were possibly caused by the inhibition of the Wnt/β-catenin pathway, indicating an underlying therapeutic prospect of SA for chondrosarcoma. Hindawi 2022-08-31 /pmc/articles/PMC9451980/ /pubmed/36091590 http://dx.doi.org/10.1155/2022/8063497 Text en Copyright © 2022 Jiamei Le et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Le, Jiamei
Ji, Houlin
Pi, Peixian
Chen, Kaijie
Gu, Xuefeng
Ma, Yujie
Fu, Yi
Sun, Yongning
Zhou, Xiaoxiao
Wu, Hailong
The Effects and Mechanisms of Sennoside A on Inducing Cytotoxicity, Apoptosis, and Inhibiting Metastasis in Human Chondrosarcoma Cells
title The Effects and Mechanisms of Sennoside A on Inducing Cytotoxicity, Apoptosis, and Inhibiting Metastasis in Human Chondrosarcoma Cells
title_full The Effects and Mechanisms of Sennoside A on Inducing Cytotoxicity, Apoptosis, and Inhibiting Metastasis in Human Chondrosarcoma Cells
title_fullStr The Effects and Mechanisms of Sennoside A on Inducing Cytotoxicity, Apoptosis, and Inhibiting Metastasis in Human Chondrosarcoma Cells
title_full_unstemmed The Effects and Mechanisms of Sennoside A on Inducing Cytotoxicity, Apoptosis, and Inhibiting Metastasis in Human Chondrosarcoma Cells
title_short The Effects and Mechanisms of Sennoside A on Inducing Cytotoxicity, Apoptosis, and Inhibiting Metastasis in Human Chondrosarcoma Cells
title_sort effects and mechanisms of sennoside a on inducing cytotoxicity, apoptosis, and inhibiting metastasis in human chondrosarcoma cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9451980/
https://www.ncbi.nlm.nih.gov/pubmed/36091590
http://dx.doi.org/10.1155/2022/8063497
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