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Vol. 59, Issue 4, 901-908, April 2001
Superfamily Member That Has Proapoptotic and Antitumorigenic Activities
Laboratory of Molecular Carcinogenesis, National Institute of
Environmental Health Sciences, National Institutes of Health, Research
Triangle Park, North Carolina
The antitumorigenic activity of nonsteroidal anti-inflammatory drugs
(NSAIDs), cyclooxygenase (COX) inhibitors, is well established, but
responsible molecular mechanisms are not fully understood. NSAIDs
stimulate apoptosis by COX dependent and independent mechanisms in
colorectal cells in culture. Identification of genes regulated by COX
inhibitors could lead to a better understanding of their proapoptotic
and anti-neoplastic activities. Using subtractive hybridization, a cDNA
which was designated as NSAID activated gene (NAG-1) was identified
from NSAID-treated HCT-116, human colorectal cells. NAG-1 has an
identical sequence with a novel member of the TGF-
superfamily that
has 5 different names. In the HCT-116 cells, NAG-1 expression is
increased and apoptosis is induced by treatment with some NSAIDs in a
concentration and time-dependent manner. NAG-1 transfected cells
exhibited increased basal apoptosis, increased response to NSAIDs and
reduced soft agar cloning efficiency. Furthermore, transplantable
tumors derived from NAG-1 transfected HCT-116 cells showed reduced
tumorigenicity in athymic nude mice compared with vector-transfected
HCT-116 cells. The increased NAG-1 expression by NSAIDs provides a
suitable explanation for COX-independent apoptotic effects of NSAIDs in cultured cells. These data demonstrate that NAG-1 is an antitumorigenic and proapoptotic protein, and its regulation by COX inhibitors may
provide new clues for explaining their proapoptotic and antitumorigenic activities.
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