scholarly journals Chrysin Attenuates Cell Viability of Human Colorectal Cancer Cells through Autophagy Induction Unlike 5-Fluorouracil/Oxaliplatin

2018 ◽  
Vol 19 (6) ◽  
pp. 1763 ◽  
Author(s):  
Yueh-Ming Lin ◽  
Chih-I Chen ◽  
Yi-Ping Hsiang ◽  
Yung-Chia Hsu ◽  
Kung-Chuan Cheng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Human Colorectal Cancer ◽  
Autophagy Induction ◽  
Colorectal Cancer Cells ◽  
Human Colorectal Cancer Cells

Vitex rotundifolia Fruit Extract Induces Apoptosis Through the Downregulation of ATF3-Mediated Bcl-2 Expression in Human Colorectal Cancer Cells

2017 ◽  
Vol 45 (04) ◽  
pp. 901-915 ◽  
Author(s):  
Hun Min Song ◽  
Gwang Hun Park ◽  
Jin Suk Koo ◽  
Hyung Jin Jeong ◽  
Jin Boo Jeong
Keyword(s):  
Colorectal Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Transcriptional Activation ◽  
Mrna Level ◽  
Human Colorectal Cancer ◽  
Colorectal Cancer Cells ◽  
Induction Of Apoptosis ◽  
Atf3 Expression ◽  
Human Colorectal Cancer Cells

Fruit from Vitex rotundifolia L. (VF) has been reported to initiate apoptosis in human colorectal cancer cells through the accumulation of reactive oxygen species. Since various regulatory factors are involved in the apoptotic pathway, further study of the potential mechanisms of VF associated with the induction of apoptosis may be important despite the fact that the molecular target of VF for apoptosis has already been elucidated. In this study, we showed a new potential mechanism for the relationship between VF-mediated ATF3 expression and apoptosis to better understand the apoptotic mechanism of VF in human colorectal cancer cells. VF reduced the cell viability and induced apoptosis in human colorectal cancer cells. VF treatment increased both the protein and mRNA level of ATF3 and upregulated ATF3 promoter activity. The cis-element responsible for ATF3 transcriptional activation by VF was CREB which is located between [Formula: see text]147 to [Formula: see text]85 of ATF3 promoter. Inhibitions of ERK1/2, p38, JNK and GSK3[Formula: see text] blocked VF-mediated ATF3 expression. ATF3 knockdown by ATF3 siRNA attenuated the cleavage of PARP by VF, while ATF3 overexpression increased VF-mediated cleaved PARP. ATF3 knockdown also attenuated VF-mediated cell viability and cell death. In addition, VF downregulated Bcl-2 expression at both protein and mRNA level. ATF3 knockdown by ATF3 siRNA blocked VF-mediated downregulation of Bcl-2. In conclusion, VF may activate ATF3 expression through transcriptional regulation and subsequently suppress Bcl-2 expression as an anti-apoptotic protein, which may result in the induction of apoptosis in human colorectal cancer cells.

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