当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > Phosphatidylinositol 5-phosphate 4-kinase type II beta is required for vitamin D receptor-dependent E-cadherin expression in SW480 cells.

Phosphatidylinositol 5-phosphate 4-kinase type II beta is required for vitamin D receptor-dependent E-cadherin expression in SW480 cells.

Abstract：

:Numerous epidemiological data indicate that vitamin D receptor (VDR) signaling induced by its ligand or active metabolite 1α,25-dihydroxyvitamin D(3) (1α,25(OH)(2)D(3)) has anti-cancer activity in several colon cancers. 1α,25(OH)(2)D(3) induces the epithelial differentiation of SW480 colon cancer cells expressing VDR (SW480-ADH) by upregulating E-cadherin expression; however, its precise mechanism remains unknown. We found that phosphatidylinositol-5-phosphate 4-kinase type II beta (PIPKIIβ) but not PIPKIIα is required for VDR-mediated E-cadherin induction in SW480-ADH cells. The syntenin-2 postsynaptic density protein/disc large/zona occludens (PDZ) domain and pleckstrin homology domain of phospholipase C-delta1 (PLCδ1 PHD) possess high affinity for phosphatidylinositol-4,5-bisphosphate (PI(4,5)P(2)) mainly localized to the nucleus and plasma membrane, respectively. The expression of syntenin-2 PDZ but not PLCδ1 PHD inhibited 1α,25(OH)(2)D(3)-induced E-cadherin upregulation, suggesting that nuclear PI(4,5)P(2) production mediates E-cadherin expression through PIPKIIβ in a VDR-dependent manner. PIPKIIβ is also involved in the suppression of the cell motility induced by 1α,25(OH)(2)D(3). These results indicate that PIPKIIβ-mediated PI(4,5)P(2) signaling is important for E-cadherin upregulation and inhibition of cellular motility induced by VDR activation.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Kouchi Z,Fujiwara Y,Yamaguchi H,Nakamura Y,Fukami K

doi

10.1016/j.bbrc.2011.04.045

subject

Has Abstract

pub_date

2011-05-20 00:00:00

pages

523-9

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(11)00619-X

journal_volume

408

pub_type

杂志文章

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