Casticin induced apoptotic cell death and altered associated gene expression in human colon cancer colo 205 cells

Hung Sheng Shang, Jia You Liu, Hsu Feng Lu, Han Sun Chiang, Chia Hain Lin, Ann Chen, Yuh Feng Lin, Jing Gung Chung

研究成果: 雜誌貢獻文章

6 引文 (Scopus)

摘要

Casticin, a polymethoxyflavone, derived from natural plant Fructus Viticis exhibits biological activities including anti-cancer characteristics. The anti-cancer and alter gene expression of casticin on human colon cancer cells and the underlying mechanisms were investigated. Flow cytometric assay was used to measure viable cell, cell cycle and sub-G1 phase, reactive oxygen species (ROS) and Ca2+ productions, level of mitochondria membrane potential (ΔΨm) and caspase activity. Western blotting assay was used to detect expression of protein level associated with cell death. Casticin induced cell morphological changes, decreased cell viability and induced G2/M phase arrest in colo 205 cells. Casticin increased ROS production but decreased the levels of ΔΨm, and Ca2+, increased caspase-3, -8, and -9 activities. The cDNA microarray indicated that some of the cell cycle associated genes were down-regulated such as cyclin-dependent kinase inhibitor 1A (CDKN1A) (p21, Cip1) and p21 protein (Cdc42/Rac)-activated kinase 3 (PAK3). TNF receptor-associated protein 1 (TRAP1), CREB1 (cAMP responsive element binding protein 1) and cyclin-dependent kinase inhibitor 1B (CDKN1B) (p27, Kip1) genes were increased but matrix metallopeptidase 2 (MMP-2), toll-like receptor 4 (TLR4), PRKAR2B (protein kinase, cAMP-dependent, regulatory, type II, bet), and CaMK4 (calcium/calmodulin-dependent protein kinase IV) genes were inhibited. Results suggest that casticin induced cell apoptosis via the activation of the caspase- and/or mitochondria-dependent signaling cascade, the accumulation of ROS and altered associated gene expressions in colo 205 human colon cancer cells.

原文英語
期刊Environmental Toxicology
DOIs
出版狀態接受/付印 - 2016

指紋

Cell death
Gene expression
Colonic Neoplasms
gene expression
cancer
Cell Death
Cells
Gene Expression
protein
Reactive Oxygen Species
Mitochondria
Cyclin-Dependent Kinase Inhibitor p27
Genes
Caspases
mitochondrion
Assays
Calcium-Calmodulin-Dependent Protein Kinase Type 4
TNF Receptor-Associated Factor 1
cdc42 GTP-Binding Protein
gene

ASJC Scopus subject areas

  • Toxicology
  • Management, Monitoring, Policy and Law
  • Health, Toxicology and Mutagenesis

引用此文

Shang, H. S., Liu, J. Y., Lu, H. F., Chiang, H. S., Lin, C. H., Chen, A., ... Chung, J. G. (認可的出版社/出版中). Casticin induced apoptotic cell death and altered associated gene expression in human colon cancer colo 205 cells. Environmental Toxicology. https://doi.org/10.1002/tox.22381

Casticin induced apoptotic cell death and altered associated gene expression in human colon cancer colo 205 cells. / Shang, Hung Sheng; Liu, Jia You; Lu, Hsu Feng; Chiang, Han Sun; Lin, Chia Hain; Chen, Ann; Lin, Yuh Feng; Chung, Jing Gung.

於: Environmental Toxicology, 2016.

研究成果: 雜誌貢獻文章

Shang, Hung Sheng ; Liu, Jia You ; Lu, Hsu Feng ; Chiang, Han Sun ; Lin, Chia Hain ; Chen, Ann ; Lin, Yuh Feng ; Chung, Jing Gung. / Casticin induced apoptotic cell death and altered associated gene expression in human colon cancer colo 205 cells. 於: Environmental Toxicology. 2016.
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abstract = "Casticin, a polymethoxyflavone, derived from natural plant Fructus Viticis exhibits biological activities including anti-cancer characteristics. The anti-cancer and alter gene expression of casticin on human colon cancer cells and the underlying mechanisms were investigated. Flow cytometric assay was used to measure viable cell, cell cycle and sub-G1 phase, reactive oxygen species (ROS) and Ca2+ productions, level of mitochondria membrane potential (ΔΨm) and caspase activity. Western blotting assay was used to detect expression of protein level associated with cell death. Casticin induced cell morphological changes, decreased cell viability and induced G2/M phase arrest in colo 205 cells. Casticin increased ROS production but decreased the levels of ΔΨm, and Ca2+, increased caspase-3, -8, and -9 activities. The cDNA microarray indicated that some of the cell cycle associated genes were down-regulated such as cyclin-dependent kinase inhibitor 1A (CDKN1A) (p21, Cip1) and p21 protein (Cdc42/Rac)-activated kinase 3 (PAK3). TNF receptor-associated protein 1 (TRAP1), CREB1 (cAMP responsive element binding protein 1) and cyclin-dependent kinase inhibitor 1B (CDKN1B) (p27, Kip1) genes were increased but matrix metallopeptidase 2 (MMP-2), toll-like receptor 4 (TLR4), PRKAR2B (protein kinase, cAMP-dependent, regulatory, type II, bet), and CaMK4 (calcium/calmodulin-dependent protein kinase IV) genes were inhibited. Results suggest that casticin induced cell apoptosis via the activation of the caspase- and/or mitochondria-dependent signaling cascade, the accumulation of ROS and altered associated gene expressions in colo 205 human colon cancer cells.",
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T1 - Casticin induced apoptotic cell death and altered associated gene expression in human colon cancer colo 205 cells

AU - Shang, Hung Sheng

AU - Liu, Jia You

AU - Lu, Hsu Feng

AU - Chiang, Han Sun

AU - Lin, Chia Hain

AU - Chen, Ann

AU - Lin, Yuh Feng

AU - Chung, Jing Gung

PY - 2016

Y1 - 2016

N2 - Casticin, a polymethoxyflavone, derived from natural plant Fructus Viticis exhibits biological activities including anti-cancer characteristics. The anti-cancer and alter gene expression of casticin on human colon cancer cells and the underlying mechanisms were investigated. Flow cytometric assay was used to measure viable cell, cell cycle and sub-G1 phase, reactive oxygen species (ROS) and Ca2+ productions, level of mitochondria membrane potential (ΔΨm) and caspase activity. Western blotting assay was used to detect expression of protein level associated with cell death. Casticin induced cell morphological changes, decreased cell viability and induced G2/M phase arrest in colo 205 cells. Casticin increased ROS production but decreased the levels of ΔΨm, and Ca2+, increased caspase-3, -8, and -9 activities. The cDNA microarray indicated that some of the cell cycle associated genes were down-regulated such as cyclin-dependent kinase inhibitor 1A (CDKN1A) (p21, Cip1) and p21 protein (Cdc42/Rac)-activated kinase 3 (PAK3). TNF receptor-associated protein 1 (TRAP1), CREB1 (cAMP responsive element binding protein 1) and cyclin-dependent kinase inhibitor 1B (CDKN1B) (p27, Kip1) genes were increased but matrix metallopeptidase 2 (MMP-2), toll-like receptor 4 (TLR4), PRKAR2B (protein kinase, cAMP-dependent, regulatory, type II, bet), and CaMK4 (calcium/calmodulin-dependent protein kinase IV) genes were inhibited. Results suggest that casticin induced cell apoptosis via the activation of the caspase- and/or mitochondria-dependent signaling cascade, the accumulation of ROS and altered associated gene expressions in colo 205 human colon cancer cells.

AB - Casticin, a polymethoxyflavone, derived from natural plant Fructus Viticis exhibits biological activities including anti-cancer characteristics. The anti-cancer and alter gene expression of casticin on human colon cancer cells and the underlying mechanisms were investigated. Flow cytometric assay was used to measure viable cell, cell cycle and sub-G1 phase, reactive oxygen species (ROS) and Ca2+ productions, level of mitochondria membrane potential (ΔΨm) and caspase activity. Western blotting assay was used to detect expression of protein level associated with cell death. Casticin induced cell morphological changes, decreased cell viability and induced G2/M phase arrest in colo 205 cells. Casticin increased ROS production but decreased the levels of ΔΨm, and Ca2+, increased caspase-3, -8, and -9 activities. The cDNA microarray indicated that some of the cell cycle associated genes were down-regulated such as cyclin-dependent kinase inhibitor 1A (CDKN1A) (p21, Cip1) and p21 protein (Cdc42/Rac)-activated kinase 3 (PAK3). TNF receptor-associated protein 1 (TRAP1), CREB1 (cAMP responsive element binding protein 1) and cyclin-dependent kinase inhibitor 1B (CDKN1B) (p27, Kip1) genes were increased but matrix metallopeptidase 2 (MMP-2), toll-like receptor 4 (TLR4), PRKAR2B (protein kinase, cAMP-dependent, regulatory, type II, bet), and CaMK4 (calcium/calmodulin-dependent protein kinase IV) genes were inhibited. Results suggest that casticin induced cell apoptosis via the activation of the caspase- and/or mitochondria-dependent signaling cascade, the accumulation of ROS and altered associated gene expressions in colo 205 human colon cancer cells.

KW - Apoptosis

KW - Casticin

KW - CDNA microarray

KW - Colo 205 cells

KW - Mitochondria

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