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Osthole induces apoptosis of the HT-29 cells via endoplasmic reticulum stress and autophagy
Endoplasmic reticulum stress (ERS) and autophagy are important pathways, which induce apoptosis of tumor cells. Osthole has been demonstrated to exert anticancer effects via the induction of apoptosis in several human colon cancer lines, but the mechanism underlying its involvement in the induction...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8371959/ https://www.ncbi.nlm.nih.gov/pubmed/34429766 http://dx.doi.org/10.3892/ol.2021.12987 |
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author | Zhou, Xing-Hua Kang, Jian Zhong, Zhen-Dong Cheng, Yue |
author_facet | Zhou, Xing-Hua Kang, Jian Zhong, Zhen-Dong Cheng, Yue |
author_sort | Zhou, Xing-Hua |
collection | PubMed |
description | Endoplasmic reticulum stress (ERS) and autophagy are important pathways, which induce apoptosis of tumor cells. Osthole has been demonstrated to exert anticancer effects via the induction of apoptosis in several human colon cancer lines, but the mechanism underlying its involvement in the induction of ERS and autophagy in the human HT-29 colorectal cancer cell line remains unknown. The present study aimed to identify the possible signaling pathways involved in osthole-induced apoptosis of HT29 cells. Methodologically, colony formation and Cell Counting Kit-8 assays were used to assess cell proliferation and viability, respectively, while flow cytometry was performed to investigate apoptosis. Signaling pathways, including apoptosis, autophagy and ERS, were also investigated in the HT-29 cell line using western blot analysis. The results demonstrated that osthole inhibited cellular proliferation and viability in a dose-dependent manner. In addition, osthole induced the expression level of proteins associated with mitochondria-mediated cell apoptosis, autophagy and ERS. The association between autophagy and ERS in osthole-induced apoptosis in the HT-29 cell line was further clarified. Inhibiting cell autophagy with the inhibitor, 3-methyladenine, suppressed osthole-induced cell apoptosis and enhanced osthole-induced ERS. By contrast, alleviating ERS with the inhibitor, 4-phenylbutyric acid attenuated osthole-induced cell apoptosis and autophagy. In conclusion, osthole could significantly suppress the proliferation and viability of the HT-29 colorectal cancer cell line and induce cell apoptosis via autophagy and ERS. Furthermore, ERS may play a more important role in osthole-induced cell apoptosis. |
format | Online Article Text |
id | pubmed-8371959 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-83719592021-08-23 Osthole induces apoptosis of the HT-29 cells via endoplasmic reticulum stress and autophagy Zhou, Xing-Hua Kang, Jian Zhong, Zhen-Dong Cheng, Yue Oncol Lett Articles Endoplasmic reticulum stress (ERS) and autophagy are important pathways, which induce apoptosis of tumor cells. Osthole has been demonstrated to exert anticancer effects via the induction of apoptosis in several human colon cancer lines, but the mechanism underlying its involvement in the induction of ERS and autophagy in the human HT-29 colorectal cancer cell line remains unknown. The present study aimed to identify the possible signaling pathways involved in osthole-induced apoptosis of HT29 cells. Methodologically, colony formation and Cell Counting Kit-8 assays were used to assess cell proliferation and viability, respectively, while flow cytometry was performed to investigate apoptosis. Signaling pathways, including apoptosis, autophagy and ERS, were also investigated in the HT-29 cell line using western blot analysis. The results demonstrated that osthole inhibited cellular proliferation and viability in a dose-dependent manner. In addition, osthole induced the expression level of proteins associated with mitochondria-mediated cell apoptosis, autophagy and ERS. The association between autophagy and ERS in osthole-induced apoptosis in the HT-29 cell line was further clarified. Inhibiting cell autophagy with the inhibitor, 3-methyladenine, suppressed osthole-induced cell apoptosis and enhanced osthole-induced ERS. By contrast, alleviating ERS with the inhibitor, 4-phenylbutyric acid attenuated osthole-induced cell apoptosis and autophagy. In conclusion, osthole could significantly suppress the proliferation and viability of the HT-29 colorectal cancer cell line and induce cell apoptosis via autophagy and ERS. Furthermore, ERS may play a more important role in osthole-induced cell apoptosis. D.A. Spandidos 2021-10 2021-08-10 /pmc/articles/PMC8371959/ /pubmed/34429766 http://dx.doi.org/10.3892/ol.2021.12987 Text en Copyright: © Zhou et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Zhou, Xing-Hua Kang, Jian Zhong, Zhen-Dong Cheng, Yue Osthole induces apoptosis of the HT-29 cells via endoplasmic reticulum stress and autophagy |
title | Osthole induces apoptosis of the HT-29 cells via endoplasmic reticulum stress and autophagy |
title_full | Osthole induces apoptosis of the HT-29 cells via endoplasmic reticulum stress and autophagy |
title_fullStr | Osthole induces apoptosis of the HT-29 cells via endoplasmic reticulum stress and autophagy |
title_full_unstemmed | Osthole induces apoptosis of the HT-29 cells via endoplasmic reticulum stress and autophagy |
title_short | Osthole induces apoptosis of the HT-29 cells via endoplasmic reticulum stress and autophagy |
title_sort | osthole induces apoptosis of the ht-29 cells via endoplasmic reticulum stress and autophagy |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8371959/ https://www.ncbi.nlm.nih.gov/pubmed/34429766 http://dx.doi.org/10.3892/ol.2021.12987 |
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