Alterations of MCF-7 human breast cancer cell after prostaglandins PGA1 and PGF2 alpha treatment.
Treatment of monolayer cultures of MCF-7 cells with prostaglandins PGA1 and PGF2 alpha inhibited cell proliferation, reduced the rate of labeled precursor incorporation into DNA, RNA, and protein, and induced morphological changes in a dose-dependent manner. The rate of [3H]thymidine incorporation was increased by PGA1 at 10(-10)-10(-8) M, while a sharp decrease was observed at 10(-6)-10(-4) M (p less than 0.05 and p less than 0.005). PGF2 alpha inhibited [3H]thymidine incorporation at all concentrations tested. Similar results were obtained for [3H]uridine incorporation with both PGs. PGA1 inhibited [3H]leucine incorporation at 10(-4) M, but increased incorporation at 10(-10)-10(-6) M. At the ultrastructural level, neither PG induced morphological alterations at 10(-12)-10(-8) M. However, at 10(-6)-10(-4) M both PGA1 and PGF2 alpha diminished the number and size of cell surface projections; some cells appeared to completely lack microvilli. Disorganization of mitochondrial cristae and increased electron density of the matrix were also evident.
Shahabi
N A
NA
Chegini
N
N
Wittliff
J L
JL
D001943:Breast Neoplasms / Q000473:pathology* / Q000648:ultrastructure; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D004261:DNA Replication / Q000187:drug effects; D004273:DNA, Neoplasm / Q000096:biosynthesis; D015237:Dinoprost; D005260:Female; D006801:Humans; D007700:Kinetics; D009363:Neoplasm Proteins / Q000096:biosynthesis; D011454:Prostaglandins A / Q000494:pharmacology*; D011460:Prostaglandins F / Q000494:pharmacology*; D012334:RNA, Neoplasm / Q000096:biosynthesis
D004273:DNA, Neoplasm; D009363:Neoplasm Proteins; D011454:Prostaglandins A; D011460:Prostaglandins F; D012334:RNA, Neoplasm; D015237:Dinoprost; C100573:prostaglandin A1