|
KMID : 0380220060390060649
|
|
Journal of Biochemistry and Molecular Biology
2006 Volume.39 No. 6 p.649 ~ p.655
|
|
|
NSAID Activated Gene (NAG-1), a Modulator of Tumorigenesis
|
|
Eling Thomas E.
Baek Seung-Joon
Shim Min-Sub
Lee Chang-Ho
|
|
|
Abstract
|
|
|
|
The NSAID activated gene (NAG-1), a member of the TGF-β superfamily, is involved in tumor progression and development. The over-expression of NAG-1 in cancer cells results in growth arrest and increase in apoptosis, suggesting that NAG-1 has anti-tumorigenic activity. This conclusion is further supported by results of experiments with transgenic mice that ubiquitously express human NAG-1. These transgenic mice are resistant to the development of intestinal tumors following treatment with azoxymethane or by introduction of a mutant APC gene. In contrast, other data suggest a pro-tumorigenic role for NAG-1, for example, high expression of NAG-1 is frequently observed in tumors. NAG-1 may be like other members of the TGF-β superfamily, acting as a tumor suppressor in the early stages, but acting pro-tumorigenic at the later stages of tumor progression. The expression of NAG-1 can be increased by treatment with drugs and chemicals documented to prevent tumor formation and development. Most notable is the increase in NAG-1 expression by the inhibitors of cyclooxygenases that prevent human colorectal cancer development. The regulation of NAG-1 is complex, but these agents act through either p53 or EGR-1 related pathways. In addition, an increase in NAG-1 is observed in inhibition of the AKT/GSK-3β pathway, suggesting NAG-1 alters cell survival. Thus, NAG-1 expression is regulated by tumor suppressor pathways and appears to modulate tumor progression.
|
|
|
KEYWORD
|
|
|
Anti-tumorigenic, Cancer, Cox inhibitor, Minmice, NAG-1, Tumor suppressor
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|
|