Implication of the PAI-1/uPA/uPAR signalosome in the antiangiogenic action of 16K prolactinHerkenne, Stéphanie ; Bajou, Khalid ; Nguyen, Ngoc-Quynh-Nhu et alPoster (2012, May 19) Detailed reference viewed: 17 (8 ULg) MicroRNA-146a, a downstream effector of 16K prolactin, is a therapeutic target and a specific biomarker for peripartum cardiomyopathyHalkein, Julie ; Tabruyn, Sébastien ; et alPoster (2012, May 19) Detailed reference viewed: 12 (4 ULg) Implication of the PAI-1/uPA/uPAR complex in the antiangiogenic action of 16K prolactinHerkenne, Stéphanie ; Dalla Valle, Antoine ; Bajou, Khalid et alPoster (2012, April) Detailed reference viewed: 13 (4 ULg) MicroRNA-146a is a causative factor and a specific biomarker for peripartum cardiomyopathyHalkein, Julie ; Tabruyn, Sébastien ; et alPoster (2012, April) Detailed reference viewed: 10 (1 ULg) Implication of the PAI-1/uPA/uPAR complex in the antiangiogenic action of 16K hPRLHerkenne, Stéphanie ; Dalla Valle, Antoine ; Bajou, Khalid et alPoster (2012) Detailed reference viewed: 34 (7 ULg) MicroRNA-146a, a downstream effector of 16kDa prolactin, impairs the endothelium-cardiomyocyte cross-talk in peripartum cardiomyopathyStruman, Ingrid ; Halkein, Julie ; Tabruyn, Sébastien et alin FASEB meeting:the Growth Hormone/Prolactin Family in Biology and Disease. (2012) Detailed reference viewed: 7 (1 ULg) The Antiangiogenic 16K Prolactin Impairs Functional Tumor Neovascularization by Inhibiting Vessel MaturationNguyen, Ngoc-Quynh-Nhu ; ; et alin PLoS ONE (2011), 6(11), 27318-27318 Background: Angiogenesis, the formation of new blood vessels from existing vasculature, plays an essential role in tumor growth, invasion, and metastasis. 16K hPRL, the antiangiogenic 16-kDa N-terminal ... [more ▼] Background: Angiogenesis, the formation of new blood vessels from existing vasculature, plays an essential role in tumor growth, invasion, and metastasis. 16K hPRL, the antiangiogenic 16-kDa N-terminal fragment of human prolactin was shown to prevent tumor growth and metastasis by modifying tumor vessel morphology. Methodology/Principal Findings: Here we investigated the effect of 16K hPRL on tumor vessel maturation and on the related signaling pathways. We show that 16K hPRL treatment leads, in a murine B16-F10 tumor model, to a dysfunctional tumor vasculature with reduced pericyte coverage, and disruption of the PDGF-B/PDGFR-B, Ang/Tie2, and Delta/Notch pathways. In an aortic ring assay, 16K hPRL impairs endothelial cell and pericyte outgrowth from the vascular ring. In addition, 16K hPRL prevents pericyte migration to endothelial cells. This event was independent of a direct inhibitory effect of 16K hPRL on pericyte viability, proliferation, or migration. In endothelial cell-pericyte cocultures, we found 16K hPRL to disturb Notch signaling. Conclusions/Significance: Taken together, our data show that 16K hPRL impairs functional tumor neovascularization by inhibiting vessel maturation and for the first time that an endogenous antiangiogenic agent disturbs Notch signaling. These findings provide new insights into the mechanisms of 16K hPRL action and highlight its potential for use in anticancer therapy. [less ▲] Detailed reference viewed: 81 (19 ULg) The antiangiogenic 16K prolactin disturbs functional tumor neovascularization by affecting vessel maturationNguyen, Ngoc-Quynh-Nhu ; ; et alPoster (2011, May) 16K hPRL, the antiangiogenic 16-kDa N-terminal fragment of human prolactin was shown to prevent tumor growth and metastasis by modifying tumor vessel morphology. Here we investigated the effect of 16K ... [more ▼] 16K hPRL, the antiangiogenic 16-kDa N-terminal fragment of human prolactin was shown to prevent tumor growth and metastasis by modifying tumor vessel morphology. Here we investigated the effect of 16K hPRL on tumor vessel maturation and on the related signaling pathways. We show that 16K hPRL treatment leads, in a murine B16-F10 tumor model, to a dysfunctional tumor vasculature with reduced pericyte coverage, and disruption of the PDGF-B/PDGFR-B, Ang/Tie2, and Delta/Notch pathways. In an aortic ring assay, 16K hPRL impairs endothelial cell and pericyte outgrowth from the vascular ring. In addition, 16K hPRL prevents pericyte migration to endothelial cells. This event was independent of a direct inhibitory effect of 16K hPRL on pericyte viability, proliferation, or migration. In endothelial cell-pericyte cocultures, we found 16K hPRL to disturb Notch signaling, this being the first time such an effect is observed with an endogenous antiangiogenic agent. These findings provide new insights into the mechanisms of 16K hPRL action and highlight its potential for use in anticancer therapy. [less ▲] Detailed reference viewed: 17 (4 ULg) Implication of the PAI-1/uPA/uPAR complex in the effects of the antiangiogenic factor 16K hPRLHerkenne, Stéphanie ; Bajou, Khalid ; D'Amico, Salvino et alPoster (2011) Detailed reference viewed: 15 (10 ULg) The antiangiogenic 16K prolactin impairs functional tumor neovascularization by affecting vessel maturationNguyen, Ngoc-Quynh-Nhu ![]() Conference (2011) Detailed reference viewed: 7 (0 ULg) Evaluation of the antitumor activity of 16K prolactin; Nguyen, Ngoc-Quynh-Nhu ; et alPoster (2009) Detailed reference viewed: 22 (14 ULg) Involvement of microRNAs in the regulation of angiogenesis by the antiangiogenic factor 16KHalkein, Julie ; ; Nguyen, Ngoc-Quynh-Nhu et alPoster (2009) Detailed reference viewed: 5 (1 ULg) Regulation of microRNAs expression by the antiangiogenic factor 16K hPRLHalkein, Julie ; ; Nguyen, Ngoc-Quynh-Nhu et alPoster (2009) Detailed reference viewed: 9 (0 ULg) The contribution of vasculogenesis to tumor neovascularization after angiostatic treatment; Nguyen, Ngoc-Quynh-Nhu ; Lecomte, Julie et alPoster (2009) Detailed reference viewed: 7 (0 ULg) Evaluation of the ability of 16K hPRL to affect tumor vessel maturationNguyen, Ngoc-Quynh-Nhu ![]() Conference (2009) Detailed reference viewed: 1 (0 ULg) The antiangiogenic factor 16K hPRL affects tumor vessel maturationNguyen, Ngoc-Quynh-Nhu ; Lion, Michelle ; Blacher, Silvia et alPoster (2009) Detailed reference viewed: 8 (3 ULg) Evaluation of the ability of 16K hPRL to affect tumor vessel maturationNguyen, Ngoc-Quynh-Nhu ; Camby, Séverine ; Lion, Michelle et alPoster (2009) Detailed reference viewed: 10 (2 ULg) Study of the effect of the antiangiogenic factor 16K hPRL in tumor vessel maturationNguyen, Ngoc-Quynh-Nhu ; Camby, Séverine ; Blacher, Silvia et alPoster (2009) Detailed reference viewed: 4 (1 ULg) Antiangiogenic liposomal gene therapy with 16K human prolactin efficiently reduces tumor growth.Kinet, Virginie ; Nguyen, Ngoc-Quynh-Nhu ; Sabatel, Céline et alin Cancer Letters (2009), 284(2), 222-228 Human 16K PRL (16K hPRL) is a potent inhibitor of angiogenesis both in vitro and in vivo. It has been shown to prevent tumor growth in three xenograft mouse models. Here we have used a gene transfer ... [more ▼] Human 16K PRL (16K hPRL) is a potent inhibitor of angiogenesis both in vitro and in vivo. It has been shown to prevent tumor growth in three xenograft mouse models. Here we have used a gene transfer method based on cationic liposomes to produce 16K hPRL and demonstrate that 16K hPRL inhibits tumor growth in a subcutaneous B16F10 mouse melanoma model. Computer-assisted image analysis shows that 16K hPRL treatment results in the reduction of tumor vessel length and width, leading to a 57% reduction in average vessel size. We thus show, for the first time, that administration of the 16K hPRL gene complexed to cationic liposomes is effective to maintain antiangiogenic activities of 16K hPRL level. [less ▲] Detailed reference viewed: 82 (34 ULg) Antiangiogenic peptidesMartial, Joseph ; Struman, Ingrid ; Nguyen, Ngoc-Quynh-Nhu et alPatent (2008) The present invention refers to a pharmaceutical composition comprising an isolated antiangiogenic peptide or a recombinant protein comprising the antiangiogenic peptide, wherein the peptide is between 11 ... [more ▼] The present invention refers to a pharmaceutical composition comprising an isolated antiangiogenic peptide or a recombinant protein comprising the antiangiogenic peptide, wherein the peptide is between 11 and 40 amino acids in length and having antiangiogenic activity, the peptide comprising the amino acid sequence: X1-X2-X3-X4-X5-X6-X7-X8-X9-X10-X11-X12-X13-X14, wherein X1 is any amino acid residue comptabile with forming a helix; X2 is an amino acid redisue of : Leu, Ile, Val; X3 is an amino acid residue of: Arg, Lys, His, Ser, Thr; X4 is an amino acid residue of: Ile, Leu, Val; X5 is any amino acid residue compatible with forming a helix; X6 is an amino acid residue of: Leu, Ile, Val; X7 is an amino acid residue of: Leu, Ile, Val, Ser, Thr; X8 is any amino acid residue compatible with forming a helix; X9 is any amino acid residue compatible with forming a helix; X10 is an amino acid residue of: Gln, Glu, Asp, Arg, His, Lys, Asn; X11 is an amino acid residue of: Ser, Thr; X12 is an amino acid residue of: Trp, Tyr, Phe; X13 is an animo acid residue of Leu, Ile, Val, Asn, Gln; X14 is an amino acid residue of: Glu, Gln, Asp, Asn. [less ▲] Detailed reference viewed: 45 (15 ULg) |
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