Regulation of SVEP1 gene expression by 17β-estradiol and TNFα in pre-osteoblastic and mammary adenocarcinoma cells

Glait-Santar, Chen; Benayahu, Dafna

doi:10.1016/j.jsbmb.2011.12.015

Cited by 16 publications

(12 citation statements)

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“…As SVEP1 normal expression was previously investigated mostly in cell lines and murine tissues, [4][5][6][9][10][11] we initially assessed its normal expression in human tissues. Using qRT-PCR, we observed ubiquitous expression of SVEP1 in a wide array of normal human tissues, with maximal expression in the placenta ( Figure 1A).…”

Section: Svep1 Is Ubiquitously Expressed In Normal Human Tissuesmentioning

confidence: 99%

“…SVEP1 has been shown to be expressed in murine placenta, lungs, intestine, stomach, skeletal tissue and preosteoblastic cells; human, murine and rat bone marrow‐derived mesenchymal stem cells; and human placenta, endothelial cells and breast cancer cell lines, while its expression has been shown to be regulated by oestrogen and tumor necrosis factor (TNF)‐α . In contrast, the pattern of expression of SVEP1 and its role in human skin remain to be determined.…”

Section: Introductionmentioning

confidence: 99%

“…[5] SVEP1 has been shown to be expressed in murine placenta, lungs, intestine, stomach, skeletal tissue and preosteoblastic cells; human, murine and rat bone marrow-derived mesenchymal stem cells; and human placenta, endothelial cells and breast cancer cell lines, while its expression has been shown to be regulated by oestrogen and tumor necrosis factor (TNF)α. [4][5][6][7][8][9][10][11][12] In contrast, the pattern of expression of SVEP1 and its role in human skin remain to be determined. Given the contribution of SVEP1 to the maintenance of cell-cell adhesion in many tissues, and the importance of adhesion molecules for skin function, we characterized SVEP1 expression and function in the epidermis.…”

Section: Introductionmentioning

confidence: 99%

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SVEP1 plays a crucial role in epidermal differentiation

Samuelov

Bochner

et al. 2017

Experimental Dermatology

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SVEP1 is a recently identified multi-domain cell adhesion protein, homologous to the mouse polydom protein, which has been shown to mediate cell-cell adhesion in an integrin dependent-manner in osteogenic cells. In the present study, we characterized SVEP1 function in the epidermis. SVEP1 was found by qRT-PCR to be ubiquitously expressed in human tissues, including the skin. Confocal microscopy revealed that SVEP1 is normally mostly expressed in the cytoplasm of basal and suprabasal epidermal cells. Down-regulation of SVEP1 expression in primary keratinocytes resulted in decreased expression of major epidermal differentiation markers. Similarly, SVEP1 down-regulation was associated with disturbed differentiation and marked epidermal acanthosis in three-dimensional skin equivalents. In contrast, the dispase assay failed to demonstrate significant differences in adhesion between keratinocytes expressing normal vs. low levels of SVEP1. Homozygous Svep1 knockout mice were embryonic lethal. Thus, to assess the importance of SVEP1 for normal skin homeostasis in vivo, we down regulated SVEP1 in zebra fish embryos with a Svep1-specific splice morpholino. Scanning electron microscopy revealed a rugged epidermis with perturbed microridge formation in the center of the keratinocytes of morphant larvae. Transmission electron microscopy analysis demonstrated abnormal epidermal cell-cell adhesion with disadhesion between cells in Svep1-deficient morphant larvae compared to controls. In summary, our results indicate that SVEP1 plays a critical role during epidermal differentiation.

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Section: Svep1 Is Ubiquitously Expressed In Normal Human Tissuesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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SVEP1 plays a crucial role in epidermal differentiation

Samuelov

Bochner

et al. 2017

Experimental Dermatology

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“…Soluble factors found to be involved in osteomimicry included BMP-2, RANKL, IGF-1, TGF-β, TNF-α, M-CSF, G-CSF, GM-CSF, 17β-estradiol, and miR218 [27,28]. These factors likely mediate the osteogenic program in cancer cells through a complex of intracellular cell signal networks involving Twist, Wnt, NF-κB, Svep-1, Rank, and c-Met [21–23,29,30]. We found that β-2m, a pleiotropic factor, regulates osteomimicry through binding to a cell-surface receptor, HFE, a hemochromatosis gene known to regulate RANKL [10,11] and iron flux in cells [31].…”

Section: Osteomimicry In the Pca Bone Metastatic Phenotype Activates mentioning

confidence: 99%

RANK-mediated signaling network and cancer metastasis

Chu

Chung

2014

Cancer Metastasis Rev

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Cancer metastasis is highly inefficient and complex. Common features of metastatic cancer cells have been observed using cancer cell lines and genetically reconstituted mouse and human tumor xenograft models. These include cancer cell interaction with the tumor microenvironment, and the ability of cancer cells to sense extracellular stimuli and adapt to adverse growth conditions. This review summarizes the coordinated response of cancer cells to soluble growth factors, such as RANKL, by a unique forward feedback mechanism employing coordinated upregulation of RANKL and c-Met with downregulation of androgen receptor. The RANK-mediated signal network was found to drive epithelial to mesenchymal transition in prostate cancer cells, promote osteomimicry and the ability of prostate cancer cells to assume stem cell and neuroendocrine phenotypes, and confer the ability of prostate cancer cells to home to bone. Prostate cancer cells with activated RANK-mediated signal network were observed to recruit and even transform the non-tumorigenic prostate cancer cells to participate in bone and soft tissue colonization. The coordinated regulation of cancer cell invasion and metastasis by the forward feedback mechanism involving RANKL, c-Met, transcription factors and VEGF-neuropilin could offer new therapeutic opportunities to target prostate cancer bone and soft tissue metastases.

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“…Previous studies have shown that several factors including RANKL, insulin‐like growth factor 1 (IGF‐1), bone morphogenetic protein 2 (BMP‐2), and transforming growth factor beta (TGFβ) were involved in acquiring an osteomimicry phenotype in prostate cancer 5,6 . These factors activate intracellular signaling molecules such as Wnt, nuclear factor κB (NF‐κB), and Twist that consequently promote the osteogenic program in PCa cells 7‐11 . RANKL‐RANK is an important signaling pathway that activates several transcription factors that have a role in multiple processes, including osteomimicry (Sox2, HIF1α, and Sox9), epithelial‐to‐mesenchymal transition (EMT and Twist1), neuroendocrine differentiation (FoxA2, Sox9, and HIF1α) and stem cell properties (Nanog and Sox2) 12 .…”

Section: Introductionmentioning

confidence: 99%

Canine prostatic cancer cell line (LuMa) with osteoblastic bone metastasis

Elshafae

Dirksen

Alasonyalilar-Demirer

et al. 2020

The Prostate

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Background: Osteoblastic bone metastasis represents the most common complication in men with prostate cancer (PCa). During progression and bone metastasis, PCa cells acquire properties similar to bone cells in a phenomenon called osteomimicry, which promotes their ability to metastasize, proliferate, and survive in the bone microenvironment. The mechanism of osteomimicry resulting in osteoblastic bone metastasis is unclear. Methods:We developed and characterized a novel canine prostatic cancer cell line (LuMa) that will be useful to investigate the relationship between osteoblastic bone metastasis and osteomimicry in PCa. The LuMa cell line was established from a primary prostate carcinoma of a 13-year old mixed breed castrated male dog. Cell proliferation and gene expression of LuMa were measured and compared to three other canine prostatic cancer cell lines (Probasco, Ace-1, and Leo) in vitro. The effect of LuMa cells on calvaria and murine preosteoblastic (MC3T3-E1) cells was measured by quantitative reverse-transcription polymerase chain reaction and alkaline phosphatase assay. LuMa cells were transduced with luciferase for monitoring in vivo tumor growth and metastasis using different inoculation routes (subcutaneous, intratibial [IT], and intracardiac [IC]). Xenograft tumors and metastases were evaluated using radiography and histopathology. Results: After left ventricular injection, LuMa cells metastasized to bone, brain, and adrenal glands. IT injections induced tumors with intramedullary new bone formation. LuMa cells had the highest messenger RNA levels of osteomimicry genes (RUNX2, RANKL, and Osteopontin [OPN]), CD44, E-cadherin, and MYOF compared to Ace-1, Probasco, and Leo cells. LuMa cells induced growth in calvaria defects and modulated gene expression in MC3T3-E1 cells. Conclusions: LuMa is a novel canine PCa cell line with osteomimicry and stemness properties. LuMa cells induced osteoblastic bone formation in vitro and in vivo.LuMa PCa cells will serve as an excellent model for studying the mechanisms of osteomimicry and osteoblastic bone and brain metastasis in prostate cancer. K E Y W O R D Sbone, canine, dog, metastasis, osteoblast, prostate cancer, tumor

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Regulation of SVEP1 gene expression by 17β-estradiol and TNFα in pre-osteoblastic and mammary adenocarcinoma cells

Cited by 16 publications

References 51 publications

SVEP1 plays a crucial role in epidermal differentiation

SVEP1 plays a crucial role in epidermal differentiation

RANK-mediated signaling network and cancer metastasis

Canine prostatic cancer cell line (LuMa) with osteoblastic bone metastasis

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