scholarly journals WISP-3 Stimulates VEGF-C-Dependent Lymphangiogenesis in Human Chondrosarcoma Cells by Inhibiting miR-196a-3p Synthesis

Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1330
Author(s):  
Chih-Yang Lin ◽  
Shih-Wei Wang ◽  
Jeng-Hung Guo ◽  
Huai-Ching Tai ◽  
Wen-Chun Sun ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Bone Tumor ◽  
Cancer Metastasis ◽  
Lymphatic Endothelial Cell ◽  
Metastatic Potential ◽  
Tube Formation ◽  
Malignant Bone Tumor ◽  
Human Chondrosarcoma ◽  
Stimulation Of

Chondrosarcoma is a malignant bone tumor with high metastatic potential. Lymphangiogenesis is a critical biological step in cancer metastasis. WNT1-inducible signaling pathway protein 3 (WISP-3) regulates angiogenesis and facilitates chondrosarcoma metastasis, but the role of WISP-3 in chondrosarcoma lymphangiogenesis is unclear. In this study, incubation of chondrosarcoma cells with WISP-3 increased the production of VEGF-C, an important lymphangiogenic factor. Conditioned medium from WISP-3-treated chondrosarcoma cells significantly enhanced lymphatic endothelial cell tube formation. WISP-3-induced stimulation of VEGF-C-dependent lymphangiogenesis inhibited miR-196a-3p synthesis in the ERK, JNK, and p38 signaling pathways. This evidence suggests that the WISP-3/VEGF-C axis is worth targeting in the treatment of lymphangiogenesis in human chondrosarcoma.

scholarly journals Novel Mechanisms of Compromised Lymphatic Endothelial Cell Homeostasis in Obesity: The Role of Leptin in Lymphatic Endothelial Cell Tube Formation and Proliferation

PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0158408 ◽  
Author(s):  
Akinori Sato ◽  
Ryuta Kamekura ◽  
Koji Kawata ◽  
Masaya Kawada ◽  
Sumito Jitsukawa ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Lymphatic Endothelial Cell ◽  
Tube Formation ◽  
Cell Homeostasis

scholarly journals Cryptotanshinone Inhibits Lymphatic Endothelial Cell Tube Formation by Suppressing VEGFR-3/ERK and Small GTPase Pathways

2011 ◽  
Vol 4 (12) ◽  
pp. 2083-2091 ◽  
Author(s):  
Yan Luo ◽  
Wenxing Chen ◽  
Hongyu Zhou ◽  
Lei Liu ◽  
Tao Shen ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Lymphatic Endothelial Cell ◽  
Tube Formation ◽  
Small Gtpase

scholarly journals Role of splice variants in the metastatic progression of prostate cancer

2012 ◽  
Vol 40 (4) ◽  
pp. 870-874 ◽  
Author(s):  
Rachel M. Hagen ◽  
Michael R. Ladomery
Keyword(s):  
Prostate Cancer ◽  
Cancer Metastasis ◽  
Splice Variants ◽  
Human Cancer ◽  
Metastatic Potential ◽  
Metastatic Progression ◽  
Cellular Phenotype ◽  
Prostate Cancer Metastasis ◽  
The Relationship

AS (alternative splicing) and its role in disease, especially cancer, has come to forefront in research over the last few years. Alterations in the ratio of splice variants have been widely observed in cancer. Splice variants of cancer-associated genes have functions that can alter cellular phenotype, ultimately altering metastatic potential. As metastases are the cause of approximately 90% of all human cancer deaths, it is crucial to understand how AS is dysregulated in metastatic disease. We highlight some recent studies into the relationship between altered AS of key genes and the initiation of prostate cancer metastasis.

Abstract P119: S100A6 Regulates Endothelial Cell Physiology

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Shumei Ren ◽  
Karsten Peppel ◽  
Patrick Most
Keyword(s):  
Cell Cycle ◽  
Endothelial Cell ◽  
Protein Function ◽  
Cell Cycle Control ◽  
Tube Formation ◽  
Cell Physiology ◽  
Ki 67 ◽  
Proliferation Markers ◽  
Serum Stimulation

Endothelial cell dysfunction is central to the development of cardiovascular pathologies. While Calcium cycling is of recognized importance to myocyte physiology and cardiac perfomance, the role of Ca2+ signaling in endothelial cell (EC) physiology remains relatively unexplored. In this study we investigated the role of S100A6 (calcyclin), an EF-hand type Ca2+ -binding protein that modulates target protein function dependent upon intracellular Ca2+ signaling. S100A6 displays cytoplasmic distribution in quiescent, confluent HUVEC, but translocates to the nucleus upon serum stimulation. Oxidative stress, induced by incubation of HUVEC with H¬2O2 (150 uM) leads to redistribution of nuclear S100A6 to the cytosol and cell cycle arrest. Knockdown of S100A6 by siRNA transfection reduced S100A6 levels by over 70% and diminished DNA synthesis by more than 75% (±12%, n=9, p<0.01), as well as expression of the proliferation markers PCNA and KI-67 (by more than 70% (±15%, n=9, p<0.01). Reduced S100A6 levels in HUVEC lead to an increase in cellular senescence, as measured by the expression of senescence associated β-galactosidase expression (by more than 6-fold, n=4, p<0.01) and a reduction of EC tube formation on matrigel matrix (by more than 90%, n=3, p<0.01). Reduction of S100A6 increased the expression of the cell cycle control and DNA repair-associated gene BRCA2, but did not change in the expression of BRCA1, cyclins or p53 (by RT-PCR array). We conclude that Ca2+ regulation by S100A6 is essential for multiple aspects of EC physiology.

scholarly journals Cathepsin B Regulates the Intrinsic Angiogenic Threshold of Endothelial Cells

2005 ◽  
Vol 16 (8) ◽  
pp. 3488-3500 ◽  
Author(s):  
Eunok Im ◽  
Annapurna Venkatakrishnan ◽  
Andrius Kazlauskas
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cathepsin B ◽  
Tube Formation ◽  
Antiangiogenic Agents ◽  
Vegf Receptor ◽  
Vegf Mrna ◽  
Lysosomal Protease ◽  
Intrinsic Capacity

The lysosomal protease cathepsin B has been implicated in a variety of pathologies including pancreatitis, tumor angiogenesis, and neuronal diseases. We used a tube formation assay to investigate the role of cathepsin B in angiogenesis. When cultured between two layers of collagen I, primary endothelial cells formed tubes in response to exogenously added VEGF. Overexpressing cathepsin B reduced the VEGF-dependent tube response, whereas pharmacologically or molecularly suppressing cathepsin B eliminated the dependence on exogenous VEGF. However, tube formation still required VEGF receptor activity, which suggested that endothelial cells generated VEGF. Indeed, VEGF mRNA and protein was detectable in cells treated with cathepsin B inhibitor, which correlated with a rise in the level of HIF-1α. In addition to boosting the level of proangiogenic factors, blocking cathepsin B activity reduced the amount of the antiangiogenic protein endostatin. Thus endothelial cells have the intrinsic capacity to generate pro- and antiangiogenic agents. These observations complement and expand our appreciation of how endothelial cell–derived proteases regulate angiogenesis.

scholarly journals Lymphatic endothelial-cell expressed ACKR3 is dispensable for postnatal lymphangiogenesis and lymphatic drainage function in mice

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0249068
Author(s):  
Elena C. Sigmund ◽  
Lilian Baur ◽  
Philipp Schineis ◽  
Jorge Arasa ◽  
Victor Collado-Diaz ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Knockout Mouse ◽  
Lymphatic Endothelial Cell ◽  
Peptide Hormone ◽  
Lymphatic Drainage ◽  
Adult Mice ◽  
Lymphatic Vasculature ◽  
Lymphatic Development ◽  
And Function

Atypical chemokine receptor ACKR3 (formerly CXCR7) is a scavenging receptor that has recently been implicated in murine lymphatic development. Specifically, ACKR3-deficiency was shown to result in lymphatic hyperplasia and lymphedema, in addition to cardiac hyperplasia and cardiac valve defects leading to embryonic lethality. The lymphatic phenotype was attributed to a lymphatic endothelial cell (LEC)-intrinsic scavenging function of ACKR3 for the vascular peptide hormone adrenomedullin (AM), which is also important during postnatal lymphangiogenesis. In this study, we investigated the expression of ACKR3 in the lymphatic vasculature of adult mice and its function in postnatal lymphatic development and function. We show that ACKR3 is widely expressed in mature lymphatics and that it exerts chemokine-scavenging activity in cultured murine skin-derived LECs. To investigate the role of LEC-expressed ACKR3 in postnatal lymphangiogenesis and function during adulthood, we generated and validated a lymphatic-specific, inducible ACKR3 knockout mouse. Surprisingly, in contrast to the reported involvement of ACKR3 in lymphatic development, our analyses revealed no contribution of LEC-expressed ACKR3 to postnatal lymphangiogenesis, lymphatic morphology and drainage function.

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