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Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells
BACKGROUND: Recently, colorectal cancer has become a more common type of tumor in the world. Research has reported that several kinds of single compounds of Chinese herbs have shown anti-tumor activity in colorectal cancer. Aloe-emodin (AE), a natural compound extract from Aloe Vera, has been discov...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6142869/ https://www.ncbi.nlm.nih.gov/pubmed/30199885 http://dx.doi.org/10.12659/MSM.908400 |
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author | Cheng, Chunsheng Dong, Weiguo |
author_facet | Cheng, Chunsheng Dong, Weiguo |
author_sort | Cheng, Chunsheng |
collection | PubMed |
description | BACKGROUND: Recently, colorectal cancer has become a more common type of tumor in the world. Research has reported that several kinds of single compounds of Chinese herbs have shown anti-tumor activity in colorectal cancer. Aloe-emodin (AE), a natural compound extract from Aloe Vera, has been discovered to suppress cell proliferation and accelerate apoptosis in a variety of tumor cells. Whether AE exerts an effect on colorectal cancer cells has not yet been investigated. MATERIAL/METHODS: In this study, we examined the impact of AE on SW620 and HT29 colorectal cancer cell lines. After treatment with various concentrations of AE (10, 20, and 40 μM), cell proliferation, cell apoptosis, reactive oxygen species (ROS) generation, cytosolic calcium level, and related gene expression were analyzed. RESULTS: Our results indicated that AE suppressed cell viability and induced cell apoptosis in SW620 and HT29 cell lines. Furthermore, both cell lines when exposed to AE generated ROS, which induces endoplasmic reticulum (ER) stress. We then detected the expression of ER stress-related proteins and cytosolic calcium levels. We found that cells exposure to AE had upregulation of unfolded protein response (UPR) proteins like glucose-related protein 78 (GRP78), phosphorylated protein kinase R (PKR)-like ER kinase (p-PERK), phosphorylated eukaryotic initiation factor-2α (p-eIF2α), and transcription factor C/EBP homologous protein (CHOP). Meanwhile, we detected an increased cytosolic calcium content followed by the upregulation of the calpain-1, calpain-2 and caspase-12. CHOP and caspase-12 are important regulatory factors leading to cell apoptosis. CONCLUSIONS: AE might serve as a candidate in the treatment of colorectal cancer through inducing ER stress-dependent apoptosis. |
format | Online Article Text |
id | pubmed-6142869 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-61428692018-09-19 Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells Cheng, Chunsheng Dong, Weiguo Med Sci Monit Lab/In Vitro Research BACKGROUND: Recently, colorectal cancer has become a more common type of tumor in the world. Research has reported that several kinds of single compounds of Chinese herbs have shown anti-tumor activity in colorectal cancer. Aloe-emodin (AE), a natural compound extract from Aloe Vera, has been discovered to suppress cell proliferation and accelerate apoptosis in a variety of tumor cells. Whether AE exerts an effect on colorectal cancer cells has not yet been investigated. MATERIAL/METHODS: In this study, we examined the impact of AE on SW620 and HT29 colorectal cancer cell lines. After treatment with various concentrations of AE (10, 20, and 40 μM), cell proliferation, cell apoptosis, reactive oxygen species (ROS) generation, cytosolic calcium level, and related gene expression were analyzed. RESULTS: Our results indicated that AE suppressed cell viability and induced cell apoptosis in SW620 and HT29 cell lines. Furthermore, both cell lines when exposed to AE generated ROS, which induces endoplasmic reticulum (ER) stress. We then detected the expression of ER stress-related proteins and cytosolic calcium levels. We found that cells exposure to AE had upregulation of unfolded protein response (UPR) proteins like glucose-related protein 78 (GRP78), phosphorylated protein kinase R (PKR)-like ER kinase (p-PERK), phosphorylated eukaryotic initiation factor-2α (p-eIF2α), and transcription factor C/EBP homologous protein (CHOP). Meanwhile, we detected an increased cytosolic calcium content followed by the upregulation of the calpain-1, calpain-2 and caspase-12. CHOP and caspase-12 are important regulatory factors leading to cell apoptosis. CONCLUSIONS: AE might serve as a candidate in the treatment of colorectal cancer through inducing ER stress-dependent apoptosis. International Scientific Literature, Inc. 2018-09-10 /pmc/articles/PMC6142869/ /pubmed/30199885 http://dx.doi.org/10.12659/MSM.908400 Text en © Med Sci Monit, 2018 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) ) |
spellingShingle | Lab/In Vitro Research Cheng, Chunsheng Dong, Weiguo Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells |
title | Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells |
title_full | Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells |
title_fullStr | Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells |
title_full_unstemmed | Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells |
title_short | Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells |
title_sort | aloe-emodin induces endoplasmic reticulum stress-dependent apoptosis in colorectal cancer cells |
topic | Lab/In Vitro Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6142869/ https://www.ncbi.nlm.nih.gov/pubmed/30199885 http://dx.doi.org/10.12659/MSM.908400 |
work_keys_str_mv | AT chengchunsheng aloeemodininducesendoplasmicreticulumstressdependentapoptosisincolorectalcancercells AT dongweiguo aloeemodininducesendoplasmicreticulumstressdependentapoptosisincolorectalcancercells |