Journal
PROSTAGLANDINS & OTHER LIPID MEDIATORS
Volume 73, Issue 1-2, Pages 111-122Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.prostaglandins.2004.01.001
Keywords
15-LOX-1; p21 (Cip/WAF1); ERK; NDGA
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Funding
- NCI NIH HHS [P01CA77839] Funding Source: Medline
- NIDDK NIH HHS [R01 DK 62112, R37 DK 47297] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P01CA077839] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK062112, R37DK047297] Funding Source: NIH RePORTER
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Currently, some controversy exists regarding the precise role of 15-lipoxygenase-1 (15-LOX-1) in colorectal carcinogenesis and other aspects of cancer biology. The aim of this study was to evaluate the effect of 15-LOX-1 on p21 (Cip/WAF 1) expression and growth regulation in human colon carcinoma cells. The effect of 13-S-hydroxyoctadecadienoic acid (HODE), a product of 15-LOX-1, on p21 (Cip/WAF 1) expression was evaluated in Caco-2 cells treated with sodium butyrate (NaBT) and/or nordihydroguaiarectic acid (NDGA), a LOX inhibitor. The effect of transfecting HCT-116 cells with 15-LOX-1 was also examined. NaBT-induced p21 (Cip/WAF 1) expression was enhanced by treatment with NDGA and 13-S-HODE reversed NaBT-induced p21 (Cip/WAF 1) expression in Caco-2 cells. Overexpression of 15-LOX-1 induced extracellular signal-related kinase (ERK) 1/2 phosphorylation, decreased p21 (Cip/WAF 1) expression, and increased HCT-116 cell growth. Treatment with NDGA decreased ERK 1/2 phosphorylation, and increased p21 (Cip/WAF 1) expression in 15-LOX-1 overexpressing HCT-116 cells. Our experimental results support the hypothesis that 15-LOX-1 may have pro-neoplastic effects during the development of colorectal cancer. (C) 2004 Elsevier Inc. All rights reserved.
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