Green tea catechin (−)-epicatechin gallate induces tumour suppressor protein ATF3 via EGR-1 activation

Cho, Kyou-Nam; Sukhthankar, Mugdha; Lee, Seong-Ho; Yoon, Joo Heon; Baek, Seung Joon

doi:10.1016/j.ejca.2007.07.020

Cited by 41 publications

(32 citation statements)

References 42 publications

(30 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is interesting that several natural products with anticancer activities have been demonstrated to induce apoptosis in cancer cells via EGR-1 induction. For example, green tea catechin, epicatechin gallate [70], and resveratrol [71] have been shown to induce apoptosis and activate EGR-1 in colorectal cancer cells. The results of our study add vitamin E δ-tocotrienol to the list of natural compounds that induce EGR-1 in cancer cells with mechanistic data.…”

Section: Discussionmentioning

confidence: 99%

EGR-1/Bax pathway plays a role in vitamin E δ-tocotrienol-induced apoptosis in pancreatic cancer cells

Wang

Husain

Zhang

et al. 2015

The Journal of Nutritional Biochemistry

View full text Add to dashboard Cite

The anticancer activity of δ-tocotrienol, a bioactive vitamin E present in whole grain cereals, annatto beans, and palm fruit, is strongly dependent on its effect on the induction of apoptosis. δ-Tocotrienol-induced apoptosis is associated with consistent induction in the expression of the pro-apoptotic protein Bax. The molecular mechanism by which δ-tocotrienol regulates Bax expression is unknown. We carried out a DNA microarray study that identified δ-tocotrienol induction of the zinc finger transcription factor, EGR-1, in pancreatic cancer cells. Here, we provide evidence linking δ-tocotrienol-induced apoptosis in pancreatic cancer cells to EGR-1 regulation of Bax expression. Forced expression of EGR-1 induces Bax expression and apoptosis in pancreatic cancer cells. In contrast, knockdown of δ-tocotrienol-induced EGR-1 by small interfering RNA attenuated δ-tocotrienol-induced Bax expression and reduced δ-tocotrienol-induced apoptosis. Further analyses showed that de novo protein synthesis was not required for δ-tocotrienol-induced EGR-1 expression, suggesting a direct effect of δ-tocotrienol on EGR-1 expression. Furthermore, a ChIP assay demonstrated that EGR-1 binds to the Bax gene promoter. Finally, δ-tocotrienol treatment induced Bax expression and activated EGR-1 in the pancreatic neoplastic cells of the PDX-Cre Kras genetically engineered model of pancreatic cancer. Our study provides the first evidence for EGR-1 as a direct target of vitamin E δ-tocotrienol, suggesting that EGR-1 may act as a pro-apoptotic factor in pancreatic cancer cells via induction of Bax.

show abstract

Section: Discussionmentioning

confidence: 99%

EGR-1/Bax pathway plays a role in vitamin E δ-tocotrienol-induced apoptosis in pancreatic cancer cells

Wang

Husain

Zhang

et al. 2015

The Journal of Nutritional Biochemistry

View full text Add to dashboard Cite

show abstract

“…The Fushi tarazu (Ftz) and CREB have been reported to be cis-acting elements in ATF3 promoter containing À147 and À85 [17]. To identify the role of each cis-acting element, each sitedeleted ATF3 promoter constructs were transfected into SW480 cells and treated with 200 lM of PCA.…”

Section: Involvement Of Creb In Pca-induced Atf3 Activationmentioning

confidence: 99%

The contribution of activating transcription factor 3 to apoptosis of human colorectal cancer cells by protocatechualdehyde, a naturally occurring phenolic compound

Lee

Park

et al. 2014

Archives of Biochemistry and Biophysics

View full text Add to dashboard Cite

“…Although the molecular mechanism of how NSAIDs increase EGR-1 expression remains to be elucidated, EGR-1 induction by NSAIDs likely affects many genes involved in pro-apoptosis pathways. EGR-1 induction may play a role in not only NSAID-induced apoptosis, but also in other anticancer compounds such as green tea [40], resveratrol [41], and PI3K inhibitor [42]. …”

Section: Cox Inhibitors Alter Protein Expression Involved In Tumorimentioning

confidence: 99%

COX inhibitors directly alter gene expression: role in cancer prevention?

Wang

Baek

Eling

2011

Cancer Metastasis Rev

Self Cite

View full text Add to dashboard Cite

Inflammation is an important contributor to the development and progression of human cancers. Inflammatory lipid metabolites, prostaglandins, formed from arachidonic acid by prostaglandin H synthases commonly called cyclooxygenases (COXs) bind to specific receptors that activate signaling pathways driving the development and progression of tumors. Inhibitors of prostaglandin formation, COX inhibitors, or nonsteroidal anti-inflammatory drugs (NSAIDs) are well documented as agents that inhibit tumor growth and with long-term use prevent tumor development. NSAIDs also alter gene expression independent of COX inhibition and these changes in gene expression also appear to contribute to the anti-tumorigenic activity of these drugs. Many NSAIDs, as illustrated by sulindac sulfide, alter gene expressions by altering the expression or phosphorylation status of the transcription factors specificity protein 1 and early growth response-1 with the balance between these two events resulting in increases or decreases in specific target genes. In this review, we have summarized and discussed the various genes altered by this mechanism after NSAID treatment and how these changes in expression relate to the anti-tumorigenic activity. A major focus of the review is on NSAID-activated gene (NAG-1) or growth differentiation factor 15. This unique member of the TGF-β superfamily is highly induced by NSAIDs and numerous drugs and chemicals with anti-tumorigenic activities. Investigations with a transgenic mouse expressing the human NAG-1 suggest it acts to suppress tumor development in several mouse models of cancer. The biochemistry and biology of NAG-1 were discussed as potential contributor to cancer prevention by COX inhibitors.

show abstract

Green tea catechin (−)-epicatechin gallate induces tumour suppressor protein ATF3 via EGR-1 activation

Cited by 41 publications

References 42 publications

EGR-1/Bax pathway plays a role in vitamin E δ-tocotrienol-induced apoptosis in pancreatic cancer cells

EGR-1/Bax pathway plays a role in vitamin E δ-tocotrienol-induced apoptosis in pancreatic cancer cells

The contribution of activating transcription factor 3 to apoptosis of human colorectal cancer cells by protocatechualdehyde, a naturally occurring phenolic compound

COX inhibitors directly alter gene expression: role in cancer prevention?

Contact Info

Product

Resources

About