Compounds > 12-hydroxy-5-8-10-14-eicosatetraenoic-acid

12-hydroxy-5-8-10-14-eicosatetraenoic-acid and Carcinoma-256--Walker

12-hydroxy-5-8-10-14-eicosatetraenoic-acid has been researched along with Carcinoma-256--Walker* in 1 studies

Other Studies

1 other study(ies) available for 12-hydroxy-5-8-10-14-eicosatetraenoic-acid and Carcinoma-256--Walker

Article	Year
12(S)-HETE promotes tumor-cell adhesion by increasing surface expression of alpha V beta 3 integrins on endothelial cells. International journal of cancer, 1993, Apr-22, Volume: 54, Issue:1 The present work was undertaken to investigate the regulatory role of 12(S)-HETE, a lipoxygenase metabolite of arachidonic acid, in the surface expression of alpha v beta 3 integrin receptors in endothelial cells (rat aortic endothelial cells, or RAEC). Several monoclonal and polyclonal antibodies localized alpha v beta 3 in focal adhesions in both subconfluent and post-confluent RAEC. RAEC alpha v beta 3 integrins were further characterized by immunoblotting and immunoprecipitation. 12(S)-HETE, but not 12(R)-HETE or other lipoxygenase-derived hydroxy fatty acids, induced a dose-dependent increase in alpha v beta 3 surface expression in RAEC, which was antagonized by prostacyclin or its analog iloprost as well as by 13-HODE, a 15-lipoxygenase product of linoleic acid. 12(S)-HETE promoted RAEC adhesion to vitronectin, an effect inhibited by antibodies against alpha v beta 3. 12(S)-HETE also promoted tumor-cell (W256 carcinosarcoma) adhesion to vitronectin, which was inhibited by various antibodies against alpha IIb beta 3 but not by an antibody against alpha v. W256 adhesion to 12(S)-HETE-treated RAEC demonstrated a significant increase, which was inhibited by anti-alpha v, -beta 3, or -alpha v beta 3 antibodies and by 13-HODE. Western blotting, immunoprecipitation and reverse transcription-polymerase chain reaction indicated that W256 carcinosarcoma cells expressed alpha IIb beta 3 integrins but not alpha v beta 3. The results suggest that the lipoxygenase metabolites [i.e., 12(S)-HETE and 13-HODE] play a significant role in modulating tumor-cell interactions with endothelium by enhancing endothelial cell integrin (e.g., alpha v beta 3) expression. Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Actin Cytoskeleton; Animals; Base Sequence; Blotting, Western; Carcinoma 256, Walker; Cell Adhesion; Cell Compartmentation; Cell Membrane; Endothelium, Vascular; Gene Expression; Hydroxyeicosatetraenoic Acids; In Vitro Techniques; Integrins; Molecular Sequence Data; Oligodeoxyribonucleotides; Rats; RNA, Messenger	1993

Article

Year

12(S)-HETE promotes tumor-cell adhesion by increasing surface expression of alpha V beta 3 integrins on endothelial cells.

International journal of cancer, 1993, Apr-22, Volume: 54, Issue:1

The present work was undertaken to investigate the regulatory role of 12(S)-HETE, a lipoxygenase metabolite of arachidonic acid, in the surface expression of alpha v beta 3 integrin receptors in endothelial cells (rat aortic endothelial cells, or RAEC). Several monoclonal and polyclonal antibodies localized alpha v beta 3 in focal adhesions in both subconfluent and post-confluent RAEC. RAEC alpha v beta 3 integrins were further characterized by immunoblotting and immunoprecipitation. 12(S)-HETE, but not 12(R)-HETE or other lipoxygenase-derived hydroxy fatty acids, induced a dose-dependent increase in alpha v beta 3 surface expression in RAEC, which was antagonized by prostacyclin or its analog iloprost as well as by 13-HODE, a 15-lipoxygenase product of linoleic acid. 12(S)-HETE promoted RAEC adhesion to vitronectin, an effect inhibited by antibodies against alpha v beta 3. 12(S)-HETE also promoted tumor-cell (W256 carcinosarcoma) adhesion to vitronectin, which was inhibited by various antibodies against alpha IIb beta 3 but not by an antibody against alpha v. W256 adhesion to 12(S)-HETE-treated RAEC demonstrated a significant increase, which was inhibited by anti-alpha v, -beta 3, or -alpha v beta 3 antibodies and by 13-HODE. Western blotting, immunoprecipitation and reverse transcription-polymerase chain reaction indicated that W256 carcinosarcoma cells expressed alpha IIb beta 3 integrins but not alpha v beta 3. The results suggest that the lipoxygenase metabolites [i.e., 12(S)-HETE and 13-HODE] play a significant role in modulating tumor-cell interactions with endothelium by enhancing endothelial cell integrin (e.g., alpha v beta 3) expression.

Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Actin Cytoskeleton; Animals; Base Sequence; Blotting, Western; Carcinoma 256, Walker; Cell Adhesion; Cell Compartmentation; Cell Membrane; Endothelium, Vascular; Gene Expression; Hydroxyeicosatetraenoic Acids; In Vitro Techniques; Integrins; Molecular Sequence Data; Oligodeoxyribonucleotides; Rats; RNA, Messenger

1993