Fibroblast growth factor (Fgf) 23 gene transcription depends on actin cytoskeleton reorganization

Fajol, Abul; Honisch, Sabina; Zhang, Bingbing; Schmidt, Sebastian; Alkahtani, Saad; Alarifi, Saud; Läng, Florian; Stournaras, Christos; Föller, Michael

doi:10.1002/1873-3468.12096

Cited by 20 publications

(17 citation statements)

References 80 publications

(104 reference statements)

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“…Notably, vitamin D has been shown to regulate the actin cytoskeleton in numerous cell types. In osteoblast-like cells, vitamin D promotes actin polymerization as part of its transcriptional induction of fibroblast growth factor 23 (Fajol et al 2016). In endometrial cells, vitamin D treatment has also been shown to induce changes in actin architecture, through regulation of the RAc1/Pak1 axis (Zeng et al 2016).…”

Section: A Role For Vitamin D In Evt Invasion?mentioning

confidence: 99%

Vitamin D, the placenta and early pregnancy: effects on trophoblast function

Ganguly

Tamblyn

Finn-Sell

et al. 2018

Journal of Endocrinology

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Pregnancy is associated with significant changes in vitamin D metabolism, notably increased maternal serum levels of active vitamin D, 1,25-dihydroxyvitamin (1,25(OH) 2 D). This appears to be due primarily to increased renal activity of the enzyme 25-hydroxyvitamin D-1α-hydroxylase (CYP27B1) that catalyzes synthesis of 1,25(OH) 2 D, but CYP27B1 expression is also prominent in both the maternal decidua and fetal trophoblast components of the placenta. The precise function of placental synthesis of 1,25(OH) 2 D remains unclear, but is likely to involve localized tissue-specific responses with both decidua and trophoblast also expressing the vitamin D receptor (VDR) for 1,25(OH) 2 D. We have previously described immunomodulatory responses to 1,25(OH) 2 D by diverse populations of VDR-expressing cells within the decidua. The aim of the current review is to detail the role of vitamin D in pregnancy from a trophoblast perspective, with particular emphasis on the potential role of 1,25(OH) 2 D as a regulator of trophoblast invasion in early pregnancy. Vitamin D deficiency is common in pregnant women, and a wide range of studies have linked low vitamin D status to adverse events in pregnancy. To date, most of these studies have focused on adverse events later in pregnancy, but the current review will explore the potential impact of vitamin D on early pregnancy, and how this may influence implantation and miscarriage.

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Section: A Role For Vitamin D In Evt Invasion?mentioning

confidence: 99%

Vitamin D, the placenta and early pregnancy: effects on trophoblast function

Ganguly

Tamblyn

Finn-Sell

et al. 2018

Journal of Endocrinology

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“…The function of KDM2B depends on the co-operation with Polycomb Repressor Complex-2 (PRC-2) that enables MEFs to undergo immortalization [4]. KDM2B is regulated by the basic fibroblast growth factor (bFGF) in human tumors that in turn governs various tumor characteristics including cell growth, migration, invasiveness, angiogenesis and actin cytoskeleton organization [5-7]. A previous study reported control of cell migration and angiogenesis by KDM2B in HUVECs [6].…”

Section: Introductionmentioning

confidence: 99%

The Epigenetic Factor KDM2B Regulates EMT and Small GTPases in Colon Tumor Cells

Zacharopoulou

Tsapara

Kallergi

et al. 2018

Cell Physiol Biochem

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Background/Aims: The epigenetic factor KDM2B is a histone demethylase expressed in various tumors. Recently, we have shown that KDM2B regulates actin cytoskeleton organization, small Rho GTPases signaling, cell-cell adhesion and migration of prostate tumor cells. In the present study, we addressed its role in regulating EMT and small GTPases expression in colon tumor cells. Methods: We used RT-PCR for the transcriptional analysis of various genes, Western blotting for the assessment of protein expression and immunofluorescence microscopy for visualization of fluorescently labeled proteins. Results: We report here that KDM2B regulates EZH2 and BMI1 in HCT116 colon tumor cells. Knockdown of this epigenetic factor induced potent up-regulation of the protein levels of the epithelial markers E-cadherin and ZO-1, while the mesenchymal marker N-cadherin was downregulated. On the other hand, KDM2B overexpression downregulated the levels of both epithelial markers and upregulated the mesenchymal marker, suggesting control of EMT by KDM2B. In addition, RhoA, RhoB and RhoC protein levels diminished upon KDM2B-knockdown, while all three small GTPases became upregulated in KDM2B-overexpressing HCT116 cell clones. Interestingly, Rac1 GTPase level increased upon KDM2B-knockdown and diminished in KDM2B-overexpressing HCT116 colon tumor- and DU-145 prostate cancer cells. Conclusions: These results establish a clear functional role of the epigenetic factor KDM2B in the regulation of EMT and small-GTPases expression in colon tumor cells and further support the recently postulated oncogenic role of this histone demethylase in various tumors.

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“…Effects of 1α,25(OH) 2 D 3 include reorganization of actin cytoskeleton [11][12][13][14]. Apparently depending on the cell type, 1α,25(OH) 2 D 3 may either increase [11,12,14] or decrease [13] actin polymerisation.…”

Section: Introductionmentioning

confidence: 99%

“…Apparently depending on the cell type, 1α,25(OH) 2 D 3 may either increase [11,12,14] or decrease [13] actin polymerisation. Early and/or late actin restructuring, following modifications of actin polymerization dynamics equilibrium, is a cellular response initiated by various signals including growth factors and cytokines [15][16][17], hormones [18][19][20][21] and ions [22,23].…”

Section: Introductionmentioning

confidence: 99%

1α,25(OH)2D3 Induces Actin Depolymerization in Endometrial Carcinoma Cells by Targeting RAC1 and PAK1

Zeng

Salker

Zhang

et al. 2016

Cell Physiol Biochem

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Background: Cell proliferation and motility require actin reorganization, which is under control of various signalling pathways including ras-related C3 botulinum toxin substrate 1 (RAC1), p21 protein-activated kinase 1 (PAK1) and actin related protein 2 (ARP2). Tumour cell proliferation is modified by 1α,25-Dihydroxy-Vitamin D3 (1α,25(OH)₂D₃), a steroid hormone predominantly known for its role in calcium and phosphorus metabolism. The present study explored whether 1α,25(OH)₂D₃ modifies actin cytoskeleton in Ishikawa cells, a well differentiated endometrial carcinoma cell line. Methods: To this end, actin cytoskeleton was visualized by confocal microscopy. Globular over filamentous actin ratio was determined utilizing Western blotting and flow cytometry, transcript levels by qRT-PCR and protein abundance by immunoblotting. Results: A 24 hour treatment with 1α,25(OH)₂D₃ (100 nM) significantly decreased RAC1 and PAK1 transcript levels and activity, decreased ARP2 protein levels and depolymerized actin. The effect of 1α,25(OH)₂D₃ on actin polymerization was mimicked by pharmacological inhibition of RAC1 and PAK1. Conclusions: 1α,25(OH)₂D₃ leads to disruption of RAC1 and PAK1 activity with subsequent actin depolymerization of endometrial carcinoma cells.

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Fibroblast growth factor (Fgf) 23 gene transcription depends on actin cytoskeleton reorganization

Cited by 20 publications

References 80 publications

Vitamin D, the placenta and early pregnancy: effects on trophoblast function

Vitamin D, the placenta and early pregnancy: effects on trophoblast function

The Epigenetic Factor KDM2B Regulates EMT and Small GTPases in Colon Tumor Cells

1α,25(OH)2D3 Induces Actin Depolymerization in Endometrial Carcinoma Cells by Targeting RAC1 and PAK1

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