Modeling Proteolytically Driven Tumor Lymphangiogenesis

2016 ◽  
pp. 107-136 ◽  
Author(s):  
Georgios Lolas ◽  
Lasse Jensen ◽  
George C. Bourantas ◽  
Vasiliki Tsikourkitoudi ◽  
Konstantinos Syrigos
Keyword(s):  
Tumor Lymphangiogenesis

Expression Profile of VEGF-C, VEGF-D, and VEGFR-3 in Different Grades of Endometrial Cancer

2019 ◽  
Vol 20 (12) ◽  
pp. 1004-1010
Author(s):  
Marcin Oplawski ◽  
Konrad Dziobek ◽  
Nikola Zmarzły ◽  
Beniamin Grabarek ◽  
Tomasz Halski ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Optical Density ◽  
Metastatic Potential ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Tumor Lymphangiogenesis ◽  
Neoplastic Process ◽  
The One ◽  
Post Hoc ◽  
Endothelial Growth Factor

Background: Vascular endothelial growth factor (VEGF)-C, -D, and VEGF receptor-3 are proteins characterized as crucial for tumor lymphangiogenesis. It is accompanied by angiogenesis during wound healing, but also in the neoplastic process. The research studies have shown that the lymphatic system plays a key role in the progression of carcinogenesis. Objective: The aim of this study was to evaluate changes in the expression of VEGF-C, VEGF-D and VEGFR-3 in different grades of endometrial cancer (G1-G3). Methods: The study included 45 patients diagnosed with endometrial cancer (G1=17; G2=15; G3=13) and 15 patients without neoplastic changes. The expression of VEGF-C, VEGF-D, and VEGFR-3 was assessed using microarray technique and immunohistochemistry. Statistical analysis was performed using the one-way ANOVA and Tukey's post-hoc test. Results: Statistically significant changes in the expression at the transcriptome level were found only in the case of VEGF-C (G1 vs. C, fold change - FC = -1.15; G2 vs. C, FC = -2.33; G3 vs. C, FC = - 1.68). However, VEGF-D and VEGFR-3 were expressed at the protein level. Analysis of VEGF-D expression showed that the optical density of the reaction product in G1 reached 101.7, while the values in G2 and G3 were 142.7 and 184.4, respectively. For VEGF-R3, the optical density of the reaction product reached the following levels: 72 in control, 118.77 in G1, 145.8 in G2, and 170.9 in G3. Conclusion: : An increase in VEGF-D and VEGFR-3 levels may indicate that VEGF-D-dependent processes are intensified along with the dedifferentiation of tumor cells. The lack of VEGF-C expression in endometrial cancer samples may suggest that this tumor is characterized by a different mechanism of metastasis than EMT. Our study emphasizes that when analyzing the metastatic potential of cancer, the expression of more than one factor should be taken into account.

LYVE-1, the lymphatic system and tumor lymphangiogenesis

2001 ◽  
Vol 22 (6) ◽  
pp. 317-321 ◽  
Author(s):  
David G Jackson ◽  
Remko Prevo ◽  
Steven Clasper ◽  
Suneale Banerji
Keyword(s):  
Lymphatic System ◽  
Tumor Lymphangiogenesis

scholarly journals Endothelial-specific depletion of TGF-β signaling affects lymphatic function

2021 ◽  
Vol 41 (1) ◽  
Author(s):  
Kunpei Fukasawa ◽  
Kako Hanada ◽  
Kei Ichikawa ◽  
Masanori Hirashima ◽  
Takahiro Takagi ◽  
...  
Keyword(s):  
Cancer Metastasis ◽  
Transforming Growth Factor ◽  
Lymphatic Vessels ◽  
Carcinoma Cells ◽  
Conditional Knockout ◽  
Lung Carcinoma Cells ◽  
Tumor Lymphangiogenesis ◽  
Soles Of The Feet ◽  
Lewis Lung Carcinoma Cells

Abstract Background Transforming growth factor (TGF)-β is a multifunctional cytokine involved in cell differentiation, cell proliferation, and tissue homeostasis. Although TGF-β signaling is essential for maintaining blood vessel functions, little is known about the role of TGF-β in lymphatic homeostasis. Methods To delineate the role of TGF-β signaling in lymphatic vessels, TβRIIfl/fl mice were crossed with Prox1-CreERT2 mice to generate TβRIIfl/fl; Prox1-CreERT2 mice. The TβRII gene in the lymphatic endothelial cells (LECs) of the conditional knockout TβRIIiΔLEC mice was selectively deleted using tamoxifen. The effects of TβRII gene deletion on embryonic lymphangiogenesis, postnatal lymphatic structure and drainage function, tumor lymphangiogenesis, and lymphatic tumor metastasis were investigated. Results Deficiency of LEC-specific TGF-β signaling in embryos, where lymphangiogenesis is active, caused dorsal edema with dilated lymphatic vessels at E13.5. Postnatal mice in which lymphatic vessels had already been formed displayed dilation and increased bifurcator of lymphatic vessels after tamoxifen administration. Similar dilation was also observed in tumor lymphatic vessels. The drainage of FITC-dextran, which was subcutaneously injected into the soles of the feet of the mice, was reduced in TβRIIiΔLEC mice. Furthermore, Lewis lung carcinoma cells constitutively expressing GFP (LLC-GFP) transplanted into the footpads of the mice showed reduced patellar lymph node metastasis. Conclusion These data suggest that TGF-β signaling in LECs maintains the structure of lymphatic vessels and lymphatic homeostasis, in addition to promoting tumor lymphatic metastasis. Therefore, suppression of TGF-β signaling in LECs might be effective in inhibiting cancer metastasis.

893 GLUCOCORTICOIDS SUPPRESS TUMOR LYMPHANGIOGENESIS OF PROSTATE CANCER CELLS

2009 ◽  
Vol 8 (4) ◽  
pp. 344
Author(s):  
A. Yano ◽  
Y. Fujii ◽  
A. Iwai ◽  
S. Kawakami ◽  
Y. Kageyama ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Tumor Lymphangiogenesis

scholarly journals The Antitumor Effect of Gekko Sulfated Glycopeptide by Inhibiting bFGF-Induced Lymphangiogenesis

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Xiu-Li Ding ◽  
Ya-Nan Man ◽  
Jian Hao ◽  
Cui-Hong Zhu ◽  
Chang Liu ◽  
...  
Keyword(s):  
Immunohistochemical Staining ◽  
Antitumor Effect ◽  
Inhibitory Effect ◽  
Tube Formation ◽  
Fibroblast Growth ◽  
Lymphatic Endothelial Cells ◽  
Tumor Lymphangiogenesis ◽  
Extracellular Signal

Objective. To study the antilymphangiogenesis effect of Gekko Sulfated Glycopeptide (GSPP) on human lymphatic endothelial cells (hLECs).Methods. MTS was conducted to confirm the antiproliferation effect of GSPP on hLECs; flow cytometry was employed to detect hLECs cycle distribution; the antimigration effect of GSPP on hLECs was investigated by wound healing experiment and transwell experiment; tube formation assay was used to examine its inhibitory effect on the lymphangiogenesis; western blotting was conducted to detect the expression of extracellular signal-regulated kinase1/2 (Erk1/2) and p-Erk1/2 after GSPP and basic fibroblast growth factor (bFGF) treatment. Nude mice models were established to investigate the antitumor effect of GSPP in vivo. Decreased lymphangiogenesis caused by GSPP in vivo was verified by immunohistochemical staining.Results. In vitro, GSPP (10 μg/mL, 100 μg/mL) significantly inhibited bFGF-induced hLECs proliferation, migration, and tube-like structure formation (P<0.05) and antagonized the phosphorylation activation of Erk1/2 induced by bFGF. In vivo, GSPP treatment (200 mg/kg/d) not only inhibited the growth of colon carcinoma, but also inhibited the tumor lymphangiogenesis.Conclusion. GSPP possesses the antitumor ability by inhibiting bFGF-inducing lymphangiogenesis in vitro and in vivo, which may further inhibit tumor lymphatic metastasis.

LPA1/3 signaling mediates tumor lymphangiogenesis through promoting CRT expression in prostate cancer

2018 ◽  
Vol 1863 (10) ◽  
pp. 1305-1315 ◽  
Author(s):  
Yueh-Chien Lin ◽  
Chien-Chin Chen ◽  
Wei-Min Chen ◽  
Kuan-Ying Lu ◽  
Tang-Long Shen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Lymphangiogenesis

scholarly journals Parallels of Resistance between Angiogenesis and Lymphangiogenesis Inhibition in Cancer Therapy

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 762 ◽  
Author(s):  
Dennis Jones
Keyword(s):  
Cancer Progression ◽  
Focal Point ◽  
Lymphatic Vessels ◽  
Resistance Mechanisms ◽  
Angiogenic Therapy ◽  
Tumor Lymphangiogenesis ◽  
Vessel Growth ◽  
Viable Approach ◽  
Approved Drugs ◽  
Fda Approved Drugs

Metastasis is the primary cause of cancer-related mortality. Cancer cells primarily metastasize via blood and lymphatic vessels to colonize lymph nodes and distant organs, leading to worse prognosis. Thus, strategies to limit blood and lymphatic spread of cancer have been a focal point of cancer research for several decades. Resistance to FDA-approved anti-angiogenic therapies designed to limit blood vessel growth has emerged as a significant clinical challenge. However, there are no FDA-approved drugs that target tumor lymphangiogenesis, despite the consequences of metastasis through the lymphatic system. This review highlights several of the key resistance mechanisms to anti-angiogenic therapy and potential challenges facing anti-lymphangiogenic therapy. Blood and lymphatic vessels are more than just conduits for nutrient, fluid, and cancer cell transport. Recent studies have elucidated how these vasculatures often regulate immune responses. Vessels that are abnormal or compromised by tumor cells can lead to immunosuppression. Therapies designed to improve lymphatic vessel function while limiting metastasis may represent a viable approach to enhance immunotherapy and limit cancer progression.

scholarly journals Correction: SIX1 Promotes Tumor Lymphangiogenesis by Coordinating TGFβ Signals That Increase Expression of VEGF-C

2019 ◽  
Vol 79 (7) ◽  
pp. 1715-1715 ◽  
Author(s):  
Dan Liu ◽  
Li Li ◽  
Xiao-Xue Zhang ◽  
Dong-Yi Wan ◽  
Bi-Xin Xi ◽  
...  
Keyword(s):  
Tumor Lymphangiogenesis
Sign in / Sign up

Export Citation Format

Share Document