Cancer Research The Future of Cancer Research: Science and Patient Impact AACR Conference on Molecular Diagnostics - 2008
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[Cancer Research 60, 6846-6850, December 15, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

15-Lipoxygenase-1 Mediates Nonsteroidal Anti-Inflammatory Drug-induced Apoptosis Independently of Cyclooxygenase-2 in Colon Cancer Cells1

Imad Shureiqi, Dongning Chen, Reuben Lotan, Peiying Yang, Robert A. Newman, Susan M. Fischer and Scott M. Lippman2

Departments of Clinical Cancer Prevention [I. S., D. C., S. M. L.], Gastrointestinal Medical Oncology [I. S.], and Experimenal Therapeutics [P. Y., R. A. N], Carcinogenesis [S. M. F.], and Division of Cancer Prevention [R. L.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

We previously found (I. Shureiqi et al., Carcinogenesis (Lond.), 20: 1985–1995, 1999; I. Shureiqi et al., J. Natl. Cancer Inst., 92: 1136–1142, 2000) that (a) 15-lipoxygenase-1 (15-LOX-1) protein and its product 13-S-hydroxyoctadecadienoic acid (13-S-HODE) are decreased; and (b) nonsteroidal anti-inflammatory drug (NSAID)-induced 15-LOX-1 expression is critical to NSAID-induced apoptosis in colorectal cancer cells expressing cyclooxygenase-2 (COX-2). We used the NSAIDs sulindac sulfone (COX-2-independent) and NS-398 (a COX-2 inhibitor) to assess NSAID up-regulation of 15-LOX-1 in relation to COX-2 inhibition during NSAID-induced apoptosis in the DLD-1 (COX-2-negative) colon cancer cell line. We found that: (a) NSAIDs up-regulated 15-LOX-1, which preceded apoptosis; and (b) 15-LOX-1 inhibition blocked NSAID-induced apoptosis, which was restored by 13-S-HODE but not by its parent, linoleic acid. NSAIDs can induce apoptosis in colon cancer cells via up-regulation of 15-LOX-1 in the absence of COX-2.




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