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Molecular Pharmacology

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Research ArticleArticle

Cyclooxygenase Inhibitors Regulate the Expression of a TGF-β Superfamily Member That Has Proapoptotic and Antitumorigenic Activities

Seung Joon Baek, Kyung-Su Kim, Jennifer B. Nixon, Leigh C. Wilson and Thomas E. Eling
Molecular Pharmacology April 2001, 59 (4) 901-908; DOI: https://doi.org/10.1124/mol.59.4.901
Seung Joon Baek
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina
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Kyung-Su Kim
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina
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Jennifer B. Nixon
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina
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Leigh C. Wilson
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina
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Thomas E. Eling
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina
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Abstract

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-β 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.

Footnotes

    • Received October 3, 2000.
    • Accepted December 11, 2000.
  • Send reprint requests to: Dr. Thomas E. Eling, Laboratory of Molecular Carcinogenesis, 111 TW Alexander Dr., Research Triangle Park, NC 27709. E-mail: eling{at}niehs.nih.gov

  • The INDO29 sequences are deposited to GenBank with accession number AF173860.

  • U.S. Government
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Molecular Pharmacology: 59 (4)
Molecular Pharmacology
Vol. 59, Issue 4
1 Apr 2001
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Research ArticleArticle

Cyclooxygenase Inhibitors Regulate the Expression of a TGF-β Superfamily Member That Has Proapoptotic and Antitumorigenic Activities

Seung Joon Baek, Kyung-Su Kim, Jennifer B. Nixon, Leigh C. Wilson and Thomas E. Eling
Molecular Pharmacology April 1, 2001, 59 (4) 901-908; DOI: https://doi.org/10.1124/mol.59.4.901

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Research ArticleArticle

Cyclooxygenase Inhibitors Regulate the Expression of a TGF-β Superfamily Member That Has Proapoptotic and Antitumorigenic Activities

Seung Joon Baek, Kyung-Su Kim, Jennifer B. Nixon, Leigh C. Wilson and Thomas E. Eling
Molecular Pharmacology April 1, 2001, 59 (4) 901-908; DOI: https://doi.org/10.1124/mol.59.4.901
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