prostaglandin-a1 and Breast-Neoplasms

prostaglandin-a1 has been researched along with Breast-Neoplasms* in 2 studies

Other Studies

2 other study(ies) available for prostaglandin-a1 and Breast-Neoplasms

ArticleYear
Morphological alterations induced by prostaglandins E1, F2 alpha and A1 in MDA-MB-231 and MCF-7 human breast cancer cell lines.
    Cancer letters, 1987, Oct-30, Volume: 37, Issue:2

    Monolayer cultures of MDA-MB-231 and MCF-7 human breast tumor cell lines were treated with prostaglandins PGE1, PGF2 alpha and PGA1 in a concentration range of 10(-12)-10(-4) M and studied at ultrastructural level. Electron microscopic examinations of both cell lines revealed that PGE1, PGF2 alpha and PGA1 induced morphological changes at concentrations above 10(-8) M. In both the small and large MDA-MB-231 cells, deformation of mitochondrial cristae, increased density of mitochondrial matrix and accumulation of lysosomal-like vesicles were observed. In the nuclei morphological, modifications included, the presence of nuclear bodies, occasional nuclear inclusions, nucleolar budding and the disappearance of the nucleolar granular components. In MCF-7 cells, disorganization of mitochondrial cristae and an increase in their matrix density were also observed. At nuclear level, little or no morphological alterations were observed. The results also indicated that the plasma membranes of both cell lines were the most sensitive organelles to PGs action as in many cells their microvilli were either shortened and spherical in shape or absent.

    Topics: Alprostadil; Breast Neoplasms; Cell Membrane; Cyclic AMP; Dinoprost; Female; Humans; Prostaglandins A; Prostaglandins F; Tumor Cells, Cultured

1987
Alterations of MCF-7 human breast cancer cell after prostaglandins PGA1 and PGF2 alpha treatment.
    Experimental cell biology, 1987, Volume: 55, Issue:1

    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.

    Topics: Breast Neoplasms; Cell Division; Cell Line; Dinoprost; DNA Replication; DNA, Neoplasm; Female; Humans; Kinetics; Neoplasm Proteins; Prostaglandins A; Prostaglandins F; RNA, Neoplasm

1987