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Induction of Cyclooxygenase‐2 in Ras‐Transformed Human Mammary Epithelial Cells Undergoing Apoptosis
Author(s) -
NA HYEKYUNG,
SURH YOUNGJOON
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb04626.x
Subject(s) - apoptosis , celecoxib , cyclooxygenase , programmed cell death , cancer research , cell culture , chemistry , biology , microbiology and biotechnology , enzyme , pharmacology , biochemistry , genetics
A bstract : 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.