Celecoxib modulates adhesion of HT29 colon cancer cells to vascular endothelial cells by inhibiting ICAM-1 and VCAM-1 expression

The relationship between epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF) pathways in tumor growth is well established. EGF induces VEGF production in cancer cells, and the paracrine VEGF activates vascular endothelial cells to promote tumor angiogenesis and thus supports tumor cell growth in an angiogenesis-dependent manner. In this study, we found angiogenesis-independent novel crosstalk between the VEGF and the EGF pathways in the regulation of colon cancer cell proliferation. Stimulation of colon cancer cells with VEGF-A and placental growth factor (PlGF) activated VEGF receptor-1 (VEGFR-1) and increased proliferation activity in an autocrine EGF/EGF receptor (EGF-R)-dependent manner. Mechanistically, VEGFR-1 interacted with and stabilized EGF-R, leading to increased EGF-R protein levels and prolonged its expression on cell surface plasma membrane. In contrast, VEGFR-1 blockade by a neutralizing antibody and an antagonistic peptide of VEGFR-1 suppressed the complex formation of VEGFR-1 and EGF-R and decreased EGF-R expression via a lysosome-dependent pathway, resulting in the suppression of proliferation activity. Our results indicated that VEGFR-1 regulated EGF-R expression to promote proliferation activity in a cell-autonomous-dependent manner.

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Bisphenol A alters transcript levels of biomarker genes for Major Depressive Disorder in vascular endothelial cells and colon cancer cells

Chemosphere ◽

10.1016/j.chemosphere.2015.12.085 ◽

2016 ◽

Vol 153 ◽

pp. 75-77 ◽

Cited By ~ 4

Author(s):

Edna Ribeiro-Varandas ◽

H. Sofia Pereira ◽

Wanda Viegas ◽

Margarida Delgado

Keyword(s):

Colon Cancer ◽

Endothelial Cells ◽

Major Depressive Disorder ◽

Depressive Disorder ◽

Bisphenol A ◽

Vascular Endothelial Cells ◽

Vascular Endothelial ◽

Colon Cancer Cells ◽

Major Depressive ◽

Transcript Levels

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Localization of 7H6 Tight Junction-Associated Antigen along the Cell Border of Vascular Endothelial Cells Correlates with Paracellular Barrier Function against Ions, Large Molecules, and Cancer Cells

Experimental Cell Research ◽

10.1006/excr.1996.0034 ◽

1996 ◽

Vol 222 (2) ◽

pp. 269-274 ◽

Cited By ~ 65

Author(s):

Hitoshi Satoh ◽

Yun Zhong ◽

Hiroshi Isomura ◽

Masato Saitoh ◽

Katsuhiko Enomoto ◽

...

Keyword(s):

Endothelial Cells ◽

Tight Junction ◽

Cancer Cells ◽

Barrier Function ◽

Vascular Endothelial Cells ◽

Vascular Endothelial ◽

Cell Border ◽

Large Molecules

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Effects of dried longan seed (Euphoria longana Lam.) extract on VEGF secretion and expression in colon cancer cells and angiogenesis in human umbilical vein endothelial cells

Journal of Functional Foods ◽

10.1016/j.jff.2013.03.004 ◽

2013 ◽

Vol 5 (3) ◽

pp. 1088-1096 ◽

Cited By ~ 10

Author(s):

Atita Panyathep ◽

Teera Chewonarin ◽

Khanittha Taneyhill ◽

Young-Joon Surh ◽

Usanee Vinitketkumnuen

Keyword(s):

Colon Cancer ◽

Endothelial Cells ◽

Cancer Cells ◽

Umbilical Vein ◽

Colon Cancer Cells ◽

Human Umbilical Vein ◽

Longan Seed ◽

Umbilical Vein Endothelial Cells

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Calcium-channel-blockers exhibit divergent regulation of cancer extravasation through the mechanical properties of cancer cells and underlying vascular endothelial cells

Cell Biochemistry and Biophysics ◽

10.1007/s12013-021-01035-3 ◽

2021 ◽

Author(s):

S. R. Vaibavi ◽

Manoj Sivasubramaniapandian ◽

Rahul Vaippully ◽

Privita Edwina ◽

Basudev Roy ◽

...

Keyword(s):

Mechanical Properties ◽

Endothelial Cells ◽

Calcium Channel ◽

Cancer Cells ◽

Calcium Channel Blockers ◽

Vascular Endothelial Cells ◽

Channel Blockers ◽

Vascular Endothelial

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YAP Overexpression in Breast Cancer Cells Promotes Angiogenesis Through Activating Yap Signaling in Vascular Endothelial Cells

10.21203/rs.3.rs-27591/v1 ◽

2020 ◽

Author(s):

Yu Yan ◽

Qiang Song ◽

Li Yao ◽

Liang Zhao ◽

Hui Cai

Keyword(s):

Breast Cancer ◽

Endothelial Cells ◽

Cancer Cells ◽

Signaling Pathway ◽

Tumor Angiogenesis ◽

Breast Cancer Cells ◽

Vascular Endothelial Cells ◽

Tissue Growth ◽

Vascular Endothelial ◽

Potential Marker

Abstract Background:The YAP signaling pathway is altered and implicated as oncogenic in human mammary cancers.However, roles of YAP signaling that regulate the breast tumor angiogenesis have remained elusive. Tumor angiogenesis is coordinated by the activation of both cancer cells and vascular endothelial cells. Whether the YAP signalingpathway can regulate the intercellular interaction between cancer cells and endothelial cellsis essentially unknown.Results: We showed here that conditioned media from YAP overexpressed breast cancer cells (CM-YAP+) could promote angiogenesis, accompanied byincreased tube formation, migration, and proliferation of human umbilical vein endothelial cells (HUVECs). Down regulation of YAP in HUVECs reversed CM-YAP+ induced angiogenesis.CM-YAP+ time-dependently activated YAP inHUVECs by dephosphorylating YAP and increasing nuclear translocation.We also identified that both G13-RhoA and PI3K/Akt signaling pathway were necessary for CM-YAP+ induced activation of YAP.Besides, connective tissue growth factor (CTGF) and angiopoietin-2 (ANG-2)actedas down-stream of YAP in HUVECs to promote angiogenesis.In addition, subcutaneous tumors nude mice model demonstrated that tumors overexpressed YAP revealed moreneovascularization in vivo.Conclusions: YAP-YAP interaction between breastcancer cells and endothelial cellscould promote tumor angiogenesis, supporting that YAP is a potential marker and target fordeveloping novel therapeutic strategies against breast cancer.

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