scholarly journals Secreted protein acidic and rich in cysteine (SPARC) and vascular endothelial growth factor (VEGF) in endometrial cancer versus normal endometrial tissue

2020 ◽  
Vol 4 (2) ◽  
Author(s):  
Raffaella Giannice ◽  
Roberto Tozzi
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endometrial Cancer ◽  
Growth Factor ◽  
Endometrial Tissue ◽  
Secreted Protein ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Cyclooxygenase-2 expression in endometrial cancer: Correlation with microvessel count and expression of vascular endothelial growth factor and thymidine phosphorylase

2002 ◽  
Vol 33 (2) ◽  
pp. 213-219 ◽  
Author(s):  
Ritsuto Fujiwaki ◽  
Kohji Iida ◽  
Haruhiko Kanasaki ◽  
Tomoya Ozaki ◽  
Kohkichi Hata ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endometrial Cancer ◽  
Growth Factor ◽  
Thymidine Phosphorylase ◽  
Cyclooxygenase 2 ◽  
Vascular Endothelial ◽  
Microvessel Count ◽  
Endothelial Growth Factor

scholarly journals Estrogen-Induced CCN1 Is Critical for Establishment of Endometriosis-Like Lesions in Mice

2014 ◽  
Vol 28 (12) ◽  
pp. 1934-1947 ◽  
Author(s):  
Yuechao Zhao ◽  
Quanxi Li ◽  
Benita S. Katzenellenbogen ◽  
Lester F. Lau ◽  
Robert N. Taylor ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Molecular Mechanisms ◽  
Tissue Growth ◽  
Endometrial Tissue ◽  
Vascular Endothelial ◽  
Wild Type ◽  
Factor C ◽  
Endothelial Growth Factor

Endometriosis is a prevalent gynecological disorder in which endometrial tissue proliferates in extrauterine sites, such as the peritoneal cavity, eventually giving rise to painful, invasive lesions. Dysregulated estradiol (E) signaling has been implicated in this condition. However, the molecular mechanisms that operate downstream of E in the ectopic endometrial tissue are unknown. To investigate these mechanisms, we used a mouse model of endometriosis. Endometrial tissue from donor mice was surgically transplanted on the peritoneal surface of immunocompetent syngeneic recipient mice, leading to the establishment of cystic endometriosis-like lesions. Our studies revealed that treatment with E led to an approximately 3-fold increase in the lesion size within a week of transplantation. E also caused a concomitant stimulation in the expression of connective tissue growth factor/Cyr61/Nov (CCN1), a secreted cysteine-rich matricellular protein, in the lesions. Interestingly, CCN1 is highly expressed in human ectopic endometriotic lesions. To address its role in endometriosis, endometrial tissue from Ccn1-null donor mice was transplanted in wild-type recipient mice. The resulting ectopic lesions were reduced up to 75% in size compared with wild-type lesions due to diminished cell proliferation and cyst formation. Notably, loss of CCN1 also disrupted the development of vascular networks in the ectopic lesions and reduced the expression of several angiogenic factors, such as vascular endothelial growth factor-A and vascular endothelial growth factor-C. These results suggest that CCN1, acting downstream of E, critically controls cell proliferation and neovascularization, which support the growth and survival of endometriotic tissue at ectopic sites. Blockade of CCN1 signaling during the early stages of lesion establishment may provide a therapeutic avenue to control endometriosis.

Progestins suppress estrogen-induced expression of vascular endothelial growth factor (VEGF) subtypes in uterine endometrial cancer cells

1999 ◽  
Vol 141 (1-2) ◽  
pp. 63-71 ◽  
Author(s):  
Jiro Fujimoto ◽  
Hideki Sakaguchi ◽  
Reiko Hirose ◽  
Satoshi Ichigo ◽  
Teruhiko Tamaya
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endometrial Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Vascular Endothelial ◽  
Induced Expression ◽  
Uterine Endometrial Cancer ◽  
Endothelial Growth Factor

scholarly journals Suppression of lymph node and lung metastases of endometrial cancer by muscle-mediated expression of soluble vascular endothelial growth factor receptor-3

2013 ◽  
Vol 104 (8) ◽  
pp. 1107-1111 ◽  
Author(s):  
Kayoko Takahashi ◽  
Hiroaki Mizukami ◽  
Yasushi Saga ◽  
Yuji Takei ◽  
Masashi Urabe ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endometrial Cancer ◽  
Lymph Node ◽  
Growth Factor ◽  
Lung Metastases ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Secreted protein, acidic and rich in cysteine is crucial for the vascular endothelial growth factor-stimulated fibrotic process in human Tenon’s fibroblasts

2019 ◽  
Author(s):  
XiaoQiong Xiang ◽  
LiYing Luo ◽  
YuHong Chen ◽  
FuXiang Ye ◽  
Yang Fu ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Wound Healing ◽  
Growth Factor ◽  
Collagen I ◽  
Secreted Protein ◽  
Vascular Endothelial ◽  
Erk Phosphorylation ◽  
Mmp9 Expression ◽  
Fibrotic Process ◽  
Endothelial Growth Factor

Abstract Background Aberrant post-surgical scarring is responsible for failure of glaucoma filtration surgery (GFS) and is attributed to strong fibrotic process of human Tenon’s fibroblasts (HTFs). Vascular endothelial growth factor (VEGF) and secreted protein, acidic and rich in cysteine (SPARC) contribute to angiogenesis and fibrosis. However, whether SPARC can regulate the VEGF-mediated fibrotic process in HTFs has not been clarified. This study aimed to examine how SPARC and VEGF crosstalk to regulate the expression of Collagen-I and matrix metalloproteinase 9 (MMP9) as well as the ERK signalling in HTFs.Methods Human Tenon's capsule tissues were cultured for preparation of HTFs, which were characterized by immunofluorescence. The effects of VEGF treatment on SPARC, Collagen-I and MMP9 expression and ERK phosphorylation were determined by Western blot, quantitative RT-PCR and immunofluorescence. The proliferation and wound healing induced by VEGF were examined in HTFs and SPARC-silenced HTFs.Results Following successful passages, immunofluorescent assays indicated that HTFs at passages 3-9 displayed unique characters of fibroblasts with Vimentin, but not keratin, expression. Treatment with VEGF significantly up-regulated SPARC, Collagen-I and MMP9 expression and ERK phosphorylation, and promoted the proliferation and wound healing of HTFs. The stimulatory effects of VEGF were significantly mitigated by SPARC silencing in HTFs.Conclusions Our data provided novel evidence that SPARC was crucial for the VEGF-stimulated fibrotic process in HTFs and may be a novel target for anti-fibrotic therapies post GFS.

Bioinformatics Analysis of Tumor-Associated Macrophages, Vascular Endothelial Growth Factor and Microvascular Density in Endometrial Carcinomas

2020 ◽  
Vol 10 (6) ◽  
pp. 1321-1326
Author(s):  
Lili Yue ◽  
Wen Shi ◽  
Kao Li ◽  
Jingwen Shi ◽  
Yi Lian ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endometrial Cancer ◽  
Growth Factor ◽  
Myometrial Invasion ◽  
Tumor Stroma ◽  
Figo Stage ◽  
Microvascular Density ◽  
Clinicopathological Parameters ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Objective: The aim of our study was to investigate the expression of tumor-associated macrophage (TAMs), Vascular Endothelial Growth Factor (VEGF) and regional microvascular density (MVD) in different parts of the endometrial carcinoma based on bioinformatics. Methods: Immunohistochemistry assay were used to detect the density of TAMs in endometrial cancer nest, tumor stroma, and infiltrating marginal and its relationship with clinicopathological parameters, VEGF and MVD. Results: To compare with normal tissue, the TAMs in tumor stroma, cancer nest and infiltrating marginal were significantly higher. The density of TAMs in infiltrating marginal was correlated to the FIGO stage, histological grade, myometrial invasion and also lymph node metastasis in endometrial cancer; while the TAMs in tumor stroma is not related to the FIGO stage. Positive correlation between the density of TAMs in tumor stroma, infiltrating marginal and VEGF and MVD in endometrial cancer was found. Conclusion: The change of tumor microenvironment caused by increased density of TAMs promote tumor microangiogenesis and aggravate the progression of endometrial cancer.

Vascular endothelial growth factor messenger ribonucleic acid expression in human ovarian and endometrial cancer

1996 ◽  
Vol 10 (6) ◽  
pp. 375-382 ◽  
Author(s):  
N. Doldi ◽  
M. Bassan ◽  
M. Gulisano ◽  
V. Broccoli ◽  
E. Boncinelli ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endometrial Cancer ◽  
Growth Factor ◽  
Ribonucleic Acid ◽  
Vascular Endothelial ◽  
Messenger Ribonucleic Acid ◽  
Endothelial Growth Factor
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