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Ann N Y Acad Sci. 2002 Nov;973:153-60.

Induction of cyclooxygenase-2 in Ras-transformed human mammary epithelial cells undergoing apoptosis.

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Laboratory of Biochemistry and Molecular Toxicology, College of Pharmacy, Seoul National University, Seoul 151-742, Korea.


COX-2 expression has been reported to be elevated in several forms of human cancer. The presence of oncogenic ras has been associated with constitutive induction of COX-2, which confers resistance to apoptosis. Contrary to the above notion, we have found that H-ras-transformed human breast epithelial (MCF10A-ras) cells treated with the anticancer drug ET-18-O-CH(3) exhibit an increased expression of COX-2, while they still undergo apoptosis. To determine whether the induction of COX-2 by ET-18-O-CH(3) could contribute to apoptosis in MCF10A-ras cells, the selective COX-2 inhibitor celecoxib (SC-58635) was used. Celecoxib treatment attenuated ET-18-O-CH(3)-induced cell death. Taken together, the above findings suggest that COX-2 up-regulation does not necessarily confer the resistance to apoptosis in ras-transformed cells, but rather may sensitize these cells to apoptotic death.

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