Mechanism of vitamin D<sub>3</sub>‐induced transcription of phospholipase D1 in HaCat human keratinocytes

Kikuchi, Ryosuke; Sobue, Satoshi; Murakami, Masashi; Ito, Hiromi; Kimura, Ai; Iwasaki, Takashi; Shibayama, Shigehisa; Takagi, Akira; Kojima, Tetsuhito; Suzuki, Motoshi; Banno, Yoshiko; Nozawa, Yoshinori; Murate, Takashi

doi:10.1016/j.febslet.2007.03.073

Cited by 10 publications

(3 citation statements)

References 15 publications

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“…The photosynthesis of vitamin D3 occurs largely in the basal keratinocytes of the epidermis and begins with the UVB‐induced conversion of 7‐dehydrocholesterol to vitamin D3 (1). Subsequent hydroxylations of vitamin D3 in the liver and kidney yield hormonally active 1,25 dihydroxyvitamin D3 (D3), which regulates the transactivation of gene expression in human keratinocytes through a canonical pathway of complex formation with its receptor, VDR, and complex binding to vitamin D responsive elements in the promoters of genes such as phospholipase D1 (2). D3 regulates the proliferation and differentiation of keratinocytes, linking the regulation of keratinocyte homeostasis to UVB exposure.…”

Section: Introductionmentioning

confidence: 99%

Ligand‐independent Regulation of the hairless Promoter by Vitamin D Receptor^†

Engelhard

Bauer

Casta

et al. 2008

Photochem & Photobiology

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The characteristic alopecia associated with mutations in the hairless (hr) and vitamin D receptor (VDR) genes defines the resulting genetic disorders, known as atrichia and VDRRIIa rickets, as phenocopies. In both cases, the separation of the dermal papilla from the regressing hair follicle at the onset of the first catagen phase of the hair cycle and the development of dermal cysts and utricules subsequent to mutation of either gene suggests that their activities affect the same regulatory pathways. VDR functions as a hormonally activated transcription factor, and a role in transcription has been postulated for Hr due in part to its nuclear localization and homology with the GATA-1 zinc-finger domain. Therefore, we examined the hypothesis that VDR and Hr have a direct regulatory effect on each other via a transcriptional mechanism. Ectopic expression of the VDR repressed hr promoter activity in HaCaT cells and primary human keratinocytes (PHKs). While this repression occurs in the absence of 1,25 dihydroxyvitamin D3 (D3), the addition of ligand greatly augments the effect. However, we also demonstrate the rare phenomenon of ligandindependent promoter transactivation by VDR. We show that the full-length promoter is transactivated by VDR in a ligand-independent and cell type-specific manner, suggesting that direct transcriptional regulation of hr by the VDR accounts in part for the phenotypic overlap between atrichia and VDRRIIa rickets.

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Section: Introductionmentioning

confidence: 99%

Ligand‐independent Regulation of the hairless Promoter by Vitamin D Receptor^†

Engelhard

Bauer

Casta

et al. 2008

Photochem & Photobiology

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“…This enhanced PLD1 expression was found to precede the 1,25-dihydroxyvitamin D 3 -mediated increase in transglutaminase activity, but not the inhibition of DNA synthesis or induction of the expression of keratin 1 (a marker of early differentiation), suggesting a role for PLD1 in late keratinocyte differentiation (42). Subsequently, the PLD1 promoter was found to possess a vitamin D response element mediating its expression in response to 1,25-dihydroxyvitamin D 3 in the HaCaT human keratinocyte cell line (45). PLD2 has also been linked to keratinocyte differentiation.…”

Section: Phospholipase D In Keratinocytesmentioning

confidence: 96%

Preparation of Primary Cultures of Mouse Epidermal Keratinocytes and the Measurement of Phospholipase D Activity

Bailey

Choudhary

Merai

et al. 2014

Methods in Molecular Biology

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In this chapter information is provided about the outer layer of the skin, the epidermis, and the predominant cells comprising this epithelium, the keratinocytes. The evidence supporting a possible role for the lipid-metabolizing enzyme phospholipase D in regulating keratinocyte differentiation is also discussed. A detailed protocol for the preparation of primary cultures of epidermal keratinocytes from neonatal mice is described, to allow other investigators to obtain data concerning these important cells involved in forming and maintaining the mechanical and water permeability of the skin. Finally, a complete protocol for monitoring phospholipase D activity in intact cells is supplied in the hope that additional research will result in a better understanding of the role of phospholipase D in controlling keratinocyte proliferation and differentiation.

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“…The NCI-H460-LNM35 (LNM35), PC3, HEK293, and LNCaP cell lines have been previously reported. 7,18,19 These cells were maintained in RPMI 1640 medium containing 5% fetal bovine serum (FBS), unless otherwise noted, while BEAS-2B cells, an immortalized human lung epithelial cell line, were cultured in Ham's F-12 medium supplemented with 5 µg/mL bovine insulin, 5 µg/mL human transferrin, 100 nmol/L hydrocortisone, 0.2 nmol/L triiodine thyronine (Sigma), and 1% FBS. All cell lines were tested and confirmed to be free from Mycoplasma contamination.…”

Section: Cell Linesmentioning

confidence: 99%

CEBPγ facilitates lamellipodia formation and cancer cell migration through CERS6 upregulation

et al. 2021

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Ceramide synthase 6 (CERS6) promotes lung cancer metastasis by stimulating cancer cell migration. To examine the underlying mechanisms, we performed luciferase analysis of the CERS6 promoter region and identified the Y‐box as a cis‐acting element. As a parallel analysis of database records for 149 non–small‐cell lung cancer (NSCLC) cancer patients, we screened for trans‐acting factors with an expression level showing a correlation with CERS6 expression. Among the candidates noted, silencing of either CCAAT enhancer‐binding protein γ (CEBPγ) or Y‐box binding protein 1 (YBX1) reduced the CERS6 expression level. Following knockdown, CEBPγ and YBX1 were found to be independently associated with reductions in ceramide‐dependent lamellipodia formation as well as migration activity, while only CEBPγ may have induced CERS6 expression through specific binding to the Y‐box. The mRNA expression levels of CERS6, CEBPγ, and YBX1 were positively correlated with adenocarcinoma invasiveness. YBX1 expression was observed in all 20 examined clinical lung cancer specimens, while 6 of those showed a staining pattern similar to that of CERS6. The present findings suggest promotion of lung cancer migration by possible involvement of the transcription factors CEBPγ and YBX1.

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Mechanism of vitamin D₃‐induced transcription of phospholipase D1 in HaCat human keratinocytes

Cited by 10 publications

References 15 publications

Ligand‐independent Regulation of the hairless Promoter by Vitamin D Receptor^†

Ligand‐independent Regulation of the hairless Promoter by Vitamin D Receptor^†

Preparation of Primary Cultures of Mouse Epidermal Keratinocytes and the Measurement of Phospholipase D Activity

CEBPγ facilitates lamellipodia formation and cancer cell migration through CERS6 upregulation

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Mechanism of vitamin D3‐induced transcription of phospholipase D1 in HaCat human keratinocytes

Cited by 10 publications

References 15 publications

Ligand‐independent Regulation of the hairless Promoter by Vitamin D Receptor†

Ligand‐independent Regulation of the hairless Promoter by Vitamin D Receptor†

Preparation of Primary Cultures of Mouse Epidermal Keratinocytes and the Measurement of Phospholipase D Activity

CEBPγ facilitates lamellipodia formation and cancer cell migration through CERS6 upregulation

Contact Info

Product

Resources

About

Mechanism of vitamin D₃‐induced transcription of phospholipase D1 in HaCat human keratinocytes

Ligand‐independent Regulation of the hairless Promoter by Vitamin D Receptor^†

Ligand‐independent Regulation of the hairless Promoter by Vitamin D Receptor^†