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- Early growth response protein 1 upregulation and nuclear translocation by 20-benzoyloxycinnamaldehyde induces prostate cancer cell death = CB-ph의 기전 규명
- H S Kang; J Ock; H J Lee; Yu Jin Lee; Byoung-Mog Kwon; S H Hong
- Bibliographic Citation
- Cancer Letters, vol. 329, no. 2, pp. 217-227
- Publication Year
- 20-Benzoyloxycinnamaldehyde (BCA) induces apoptosis in human cancer cells through ROS generation.
BCA upregulates proapoptotic genes such as activating transcription factor 3 (ATF3), NSAID-activated
gene 1 protein (NAG-1), and growth arrest and DNA-damage-inducible protein alpha (GADD45A) in prostate
cancer cells. These genes are known to be induced by transcription factor early growth response protein
1 (EGR1). BCA induces significant EGR1 upregulation, while EGR1 knockdown decreases the
induction of these genes with concurrent alleviation of cell death by BCA. Antioxidant glutathione pretreatment
with BCA removes EGR1 expression increase, suggesting that EGR1 upregulation is dependent
on oxidative stress generated by BCA. In prostate cancer cells, EGR1 localizes in the cytoplasm; however,
BCA remarkably upregulates EGR1 nuclear translocalization, suggesting its possible effect as a transcriptional
activator. BCA induces transient upregulation of importin-7 (IPO7) which is critical for EGR1
nuclear translocation, and IPO7 knockdown led to a significant decrease in chemosensitivity to BCA.
Taken together, our findings suggest that BCA induces prostate cancer cell death via EGR1 upregulation
and nuclear translocalization, followed by activation of proapoptotic target genes.
- 2'-Benzoyloxycinnamaldehyde (BCA)Activating transcription factor 3 (ATF3)Early growth response protein 1 (EGR1)Growth arrest and DNA-damage-inducible protein alpha (GADD45A)Importin-7 (IPO7)NSAID-activated gene 1 protein (NAG-1)Prostate cancer cells
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- Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
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