Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 342, Issue 1-2, Pages 63-70Publisher
SPRINGER
DOI: 10.1007/s11010-010-0469-7
Keywords
Estrogen; Prostaglandin E2; Human colon cancer cell; COX-2; Cell motility
Categories
Funding
- Taiwan Department of Health Clinical Trial and Research Center of Excellence [DOH99-TD-B-111-004]
- Taiwan Department of Health Cancer Research Center of Excellence [DOH99-TD-C-111-005]
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Epidemiological studies demonstrate that the incidence and mortality rates of colorectal cancer in women are lower than in men. However, it is unknown if 17 beta-estradiol treatment is sufficient to inhibit prostaglandin E2 (PGE2)-induced cellular motility in human colon cancer cells. Upregulation of cyclooxygenase-2 (COX-2) is reported to associate with the development of cancer cell mobility, metastasis, and subsequent malignant tumor. After administration of inhibitors including LY294002 (Akt activation inhibitor), U0126 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor), or QNZ (NF kappa B inhibitor), we found that PGE2 treatment increases COX-2 via Akt and ERK1/2 pathways, thus promoting cellular motility in human LoVo cancer cells. We further observed that 17 beta-estradiol treatment inhibits PGE2-induced COX-2 expression and cellular motility via suppressing activation of Akt and ERK1/2 in human LoVo cancer cells. Collectively, these results suggest that 17 beta-estradiol treatment dramatically inhibits PGE2-induced progression of human LoVo colon cancer cells.
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