Compounds > 1-8-dinitro-4-5-dihydroxyanthraquinone

1-8-dinitro-4-5-dihydroxyanthraquinone and Carcinoma

1-8-dinitro-4-5-dihydroxyanthraquinone has been researched along with Carcinoma* in 1 studies

Other Studies

1 other study(ies) available for 1-8-dinitro-4-5-dihydroxyanthraquinone and Carcinoma

Article	Year
PPemd26, an anthraquinone derivative, suppresses angiogenesis via inhibiting VEGFR2 signalling. British journal of pharmacology, 2014, Volume: 171, Issue:24 Angiogenesis contributes to coronary heart disease, immune disorders and numerous malignancies. VEGF-A and its receptors (VEGFRs) play a pivotal role in regulating angiogenesis. In an effort to discover more effective inhibitors of tumour angiogenesis, we have analysed the actions of a novel anthraquinone derivative, PPemd26, and explored its anti-angiogenic mechanisms.. The effects of PPemd26 were evaluated in vitro using HUVEC cultures to assess proliferation, migration, invasion and tube formation. Immunoblotting was used to analyse phosphorylation of signalling kinases. Effects in vivo were assayed using Matrigel plug and xenograft mouse models.. PPemd26 significantly inhibited VEGF-A-induced proliferation, migration, invasion and tube formation of HUVECs. PPemd26 also attenuated VEGF-A-induced microvessel sprouting from rat aortic rings ex vivo and suppressed formation of new blood vessels in implanted Matrigel plugs in models of angiogenesis in vivo. In addition, PPemd26 inhibited VEGF-A-induced phosphorylation of VEGFR2 and its downstream protein kinases including Akt, focal adhesion kinase, ERK and Src. Furthermore, systemic administration of PPemd26 suppressed the growth of s.c. xenografts of human colon carcinoma in vivo. Histochemical analysis of the xenografts revealed a marked reduction in stainingfor the vascular marker CD31 and proliferation marker Ki-67.. This study provides evidence that PPemd26 suppressed tumour angiogenesis through inhibiting VEGFR2 signalling pathways, suggesting that PPemd26 is a potential drug candidate for developing anti-angiogenic agents for the treatment of cancer and angiogenesis-related diseases. Topics: Angiogenesis Inhibitors; Animals; Anthraquinones; Aorta; Carcinoma; Cell Movement; Cell Proliferation; Cell Survival; Colonic Neoplasms; Extracellular Signal-Regulated MAP Kinases; Focal Adhesion Protein-Tyrosine Kinases; Human Umbilical Vein Endothelial Cells; Humans; In Vitro Techniques; Mice; Microvessels; Neovascularization, Physiologic; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins pp60(c-src); Rats; Signal Transduction; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Xenograft Model Antitumor Assays	2014

Article

Year

PPemd26, an anthraquinone derivative, suppresses angiogenesis via inhibiting VEGFR2 signalling.

British journal of pharmacology, 2014, Volume: 171, Issue:24

Angiogenesis contributes to coronary heart disease, immune disorders and numerous malignancies. VEGF-A and its receptors (VEGFRs) play a pivotal role in regulating angiogenesis. In an effort to discover more effective inhibitors of tumour angiogenesis, we have analysed the actions of a novel anthraquinone derivative, PPemd26, and explored its anti-angiogenic mechanisms.. The effects of PPemd26 were evaluated in vitro using HUVEC cultures to assess proliferation, migration, invasion and tube formation. Immunoblotting was used to analyse phosphorylation of signalling kinases. Effects in vivo were assayed using Matrigel plug and xenograft mouse models.. PPemd26 significantly inhibited VEGF-A-induced proliferation, migration, invasion and tube formation of HUVECs. PPemd26 also attenuated VEGF-A-induced microvessel sprouting from rat aortic rings ex vivo and suppressed formation of new blood vessels in implanted Matrigel plugs in models of angiogenesis in vivo. In addition, PPemd26 inhibited VEGF-A-induced phosphorylation of VEGFR2 and its downstream protein kinases including Akt, focal adhesion kinase, ERK and Src. Furthermore, systemic administration of PPemd26 suppressed the growth of s.c. xenografts of human colon carcinoma in vivo. Histochemical analysis of the xenografts revealed a marked reduction in stainingfor the vascular marker CD31 and proliferation marker Ki-67.. This study provides evidence that PPemd26 suppressed tumour angiogenesis through inhibiting VEGFR2 signalling pathways, suggesting that PPemd26 is a potential drug candidate for developing anti-angiogenic agents for the treatment of cancer and angiogenesis-related diseases.

Topics: Angiogenesis Inhibitors; Animals; Anthraquinones; Aorta; Carcinoma; Cell Movement; Cell Proliferation; Cell Survival; Colonic Neoplasms; Extracellular Signal-Regulated MAP Kinases; Focal Adhesion Protein-Tyrosine Kinases; Human Umbilical Vein Endothelial Cells; Humans; In Vitro Techniques; Mice; Microvessels; Neovascularization, Physiologic; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins pp60(c-src); Rats; Signal Transduction; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Xenograft Model Antitumor Assays

2014