Anterograde Trafficking of CXCR4 and CCR2 Receptors in a Prostate Cancer Cell Line

Gillies, Kelsie; Wertman, Jaime; Charette, Nicholle; Dupré, Denis J.

doi:10.1159/000350126

Cited by 18 publications

(14 citation statements)

References 40 publications

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“…As a regulator of focal adhesion dynamics, FAK plays an important role in vascular endothelial mechano-transduction induced by various stimuli [77,78,79,80,81] and contributes to the regulation of vascular cell proliferation and apoptosis [39,41,82,83,84], tissue remodelling [85,86], angiogenesis and cell migration [82,87,88], leukocyte adhesion and vascular inflammation [89] as well as endothelial barrier function [82,90]. Therefore, by regulating the activity of FAK, chorein may contribute to regulation of other physiological processes beyond regulating actin polymerization and cell stiffness.…”

Section: Discussionmentioning

confidence: 99%

Chorein Sensitivity of Actin Polymerization, Cell Shape and Mechanical Stiffness of Vascular Endothelial Cells

Alesutan¹,

Seifert

Pakladok³

et al. 2013

Cell Physiol Biochem

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Background/Aims: Endothelial cell stiffness plays a key role in endothelium-dependent control of vascular tone and arterial blood pressure. Actin polymerization and distribution of microfilaments is essential for mechanical cell stiffness. Chorein, a protein encoded by the VPS13A gene, defective in chorea-acanthocytosis (ChAc), is involved in neuronal cell survival as well as cortical actin polymerization of erythrocytes and blood platelets. Chorein is expressed in a wide variety of further cells, yet nothing is known about the impact of chorein on cells other than neurons, erythrocytes and platelets. The present study explored whether chorein is expressed in human umbilical vein endothelial cells (HUVECs) and addressed the putative role of chorein in the regulation of cytoskeletal architecture, stiffness and survival of those cells. Methods: In HUVECs with or without silencing of the VPS13A gene, VPS13A mRNA expression was determined utilizing quantitative RT-PCR, cytoskeletal organization visualized by confocal microscopy, G/F actin ratio and phosphorylation status of focal adhesion kinase quantified by western blotting, cell death determined by flow cytometry, mechanical properties studied by atomic force microscopy (AFM) and cell morphology analysed by scanning ion conductance microscopy (SICM). Results: VPS13A mRNA expression was detectable in HUVECs. Silencing of the VPS13A gene attenuated the filamentous actin network, decreased the ratio of soluble G-actin over filamentous F-actin, reduced cell stiffness and changed cell morphology as compared to HUVECs silenced with negative control siRNA. These effects were paralleled by a significant decrease in FAK phosphorylation following VPS13A silencing. Moreover, silencing of the VPS13A gene increased caspase 3 activity and induced necrosis in HUVECs. Conclusions: Chorein is a novel regulator of cytoskeletal architecture, cell shape, mechanical stiffness and survival of vascular endothelial cells.

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Section: Discussionmentioning

confidence: 99%

Chorein Sensitivity of Actin Polymerization, Cell Shape and Mechanical Stiffness of Vascular Endothelial Cells

Alesutan¹,

Seifert

Pakladok³

et al. 2013

Cell Physiol Biochem

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“…The most evidence of chemokine receptors endogenously expressed by cancer cells is provided for CXCR1, CXCR2, CXCR4, and CXCR7 but also other receptors such as CCR1, CCR2, CCR3, CCR5, CCR7, CCR9, CXCR3, CXCR6, CXCR5, CX3CR1 are involved in the multistep process of prostate cancer progression and metastasis [78,[87][88][89][90][91][92]. Mainly, the work on chemokines in prostate cancer has focused on not only the chemokines CXCL8, CXCL12, and CCL2 but also other chemokines such as CCL2, CCL4, CCL5, CCL9, CCL11, CCL18, CXCL1, CXCL2, CXCL5, CXCL6, CXCL12, and CXCL13 that appear to be produced by stromal cells, endothelial cells and human bone marrow endothelial cells, differentiated osteoblasts, and infiltrating leukocytes [78,[93][94][95][96][97][98][99].…”

Section: Chemokines and Prostate Cancermentioning

confidence: 99%

Inflammation and prostate cancer: friends or foe?

Taverna

Pedretti

et al. 2015

Inflamm. Res.

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There are growing evidences that chronic inflammation is involved in the regulation of cellular events in prostate carcinogenesis, including disruption of the immune response and regulation of the tumor microenvironment. This review discusses the role played by the innate and adaptive immune system in the local progression of prostate cancer, and the prognostic information that we can currently understand and exploit.

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“…However, aggressive PCs capable of invasion do occur, in which the primary cancer cells migrate and seed to distal organs and lymph nodes [1][2][3][4]. Since the current treatments upon PCs are not sufficient to provide satisfactory therapy for aggressive PCs, further comprehension of PC metastasis is highly appreciated [1][2][3][4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

MiR-323 Inhibits Prostate Cancer Vascularization Through Adiponectin Receptor

Gao

Yao

Zheng

2015

Cell Physiol Biochem

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Background/Aims: The current treatments fail to provide satisfactory cure for aggressive prostate cancers (PCs). Hence, further comprehension of PC metastasis is highly appreciated for improving the levels of therapy. We have previously shown that Adiponectin reduces the levels of vascular endothelial growth factor A (VEGF-A) in PCs to suppress tumor-associated neovascularization, possibly through AMPK/mTor signaling. Here, we studied the regulation of Adiponectin signaling in PCs. Methods: We analyzed the levels and correlation of Adiponectin receptor 1 (AdipoR1) and microRNA-323 (miR-323) in the PC specimen, compared to the paired normal prostate tissue. We analyzed the binding of miR-323 to the 3'UTR of AdipoR1 mRNA and its effects on AdipoR1 translation by bioinformatics analysis and by luciferase-reporter assay, respectively. We modified miR-323 levels in PC cells, and examined the effects on the expression of AdipoR1 and VEGF-A, as well as on vessel formation in a human umbilical vein endothelial cells (HUVECs) transwell collagen gel assay. Results: We detected significantly lower levels of AdipoR1 and significantly higher levels of miR-323 in PC specimen. Moreover, the levels of AdipoR1 and miR-323 are inversely correlated. Moreover, miR-323 was found to bind to the 3'UTR of AdipoR1 mRNA to inhibit its translation. Overexpression of miR-323 in PC cells decreased AdipoR1 protein levels, whereas inhibition of miR-323 increased AdipoR1 protein levels, without affecting AdipoR1 transcripts. Moreover, overexpression of miR-323 increased the levels of VEGF-A and the vessel formation by HUVECs, while inhibition of miR-323 decreased the levels of VEGF-A and the vessel formation by HUVECs. Conclusion: Our data demonstrate that miR-323 may increase VEGF-A-mediated cancer vascularization in PC cells through AdipoR1 suppression.

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Anterograde Trafficking of CXCR4 and CCR2 Receptors in a Prostate Cancer Cell Line

Cited by 18 publications

References 40 publications

Chorein Sensitivity of Actin Polymerization, Cell Shape and Mechanical Stiffness of Vascular Endothelial Cells

Chorein Sensitivity of Actin Polymerization, Cell Shape and Mechanical Stiffness of Vascular Endothelial Cells

Inflammation and prostate cancer: friends or foe?

MiR-323 Inhibits Prostate Cancer Vascularization Through Adiponectin Receptor

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