(Natural News) Scientists from South Korea evaluated the apoptotic mechanism of Vitex rotundifolia L. fruit extract against human colorectal cancer cells. Their findings were published in The American Journal of Chinese Medicine.
- The fruit of V. rotundifolia or beach vitex has been reported to induce apoptosis in human colorectal cancer cells through the accumulation of oxygen species.
- The researchers aimed to further understand the mechanisms of V. rotundifolia that induce apoptosis despite the fact that the molecular target for apoptosis has already been established.
- In this study, they showed a new potential mechanism for the relationship between V. rotundifolia-mediated ATF3 expression and apoptosis in human colorectal cancer cells.
- V. rotundifolia reduced cell viability and induced apoptosis, while increasing both protein and mRNA level of ATF3 and upregulated ATF3 promoted activity.
- The cis-element responsible for ATF3 transcriptional activation by V. rotundifolia was CREB which is located between -147 to -85 of ATF3 promoter.
- Inhibitions of ERK1/2, p38, JNK and GSK3-beta blocked V. rotundifolia-mediated ATF3 expression.
- ATF3 knockdown by ATF3 siRNA reduced the cleavage of PARP by V. rotundifolia, while ATF3 overexpression increased V. rotundifolia-mediated cleaved PARP. ATF3 knockdown also decreased V. rotundifolia-mediated cell viability and cell death.
- V. rotundifolia downregulated Bcl-2 expression at both protein and mRNA level. ATF3 knockdown by ATF3 siRNA blocked V. rotundifolia-mediated downregulation of Bcl-2.
Based on these findings, the researchers conclude that V. rotundifolia induces apoptosis in human colorectal cancer cells by activating ATF3 expression through transcriptional regulation and subsequently suppresses Bcl-2 expression as an anti-apoptotic protein.
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Song HM, Park GH, Koo JS, Jeong HJ, Jeong JB. VITEX ROTUNDIFOLIA FRUIT EXTRACT INDUCES APOPTOSIS THROUGH THE DOWNREGULATION OF ATF3-MEDIATED BCL-2 EXPRESSION IN HUMAN COLORECTAL CANCER CELLS. The American Journal of Chinese Medicine. 2017;45(04):901–915. DOI: 10.1142/s0192415x17500483