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Stable knockdown of Kif5b in MDCK cells leads to epithelial-mesenchymal transition.

Abstract：

:Polarization of epithelial cells requires vectorial sorting and transport of polarity proteins to apical or basolateral domains. Kif5b is the mouse homologue of the human ubiquitous Kinesin Heavy Chain (uKHC). To investigate the function of Kif5b in epithelial cells, we examined the phenotypes of Kif5b-deficient MDCK cells. Stable knockdown of Kif5b in MDCK cells resulted in reduced cell proliferation rate, profound changes in cell morphology, loss of epithelial cell marker, and gain of mesenchymal marker, as well as increased cell migration, invasion, and tumorigenesis abilities. E-cadherin and NMMIIA could interact with Kif5b in polarized MDCK cells, and their expression levels were decreased in Kif5b-deficient MDCK cells. Overexpression of E-cadherin and NMMIIA in Kif5b depleted MDCK cells could decrease mesenchymal marker expression and cell migration ability. These results indicate that stable knockdown of Kif5b in MDCK cells can lead to epithelial-mesenchymal transition, which is mediated by defective E-cadherin and NMMIIA expression.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Cui J,Jin G,Yu B,Wang Z,Lin R,Huang JD

doi

10.1016/j.bbrc.2015.05.045

subject

Has Abstract

pub_date

2015-07-17 00:00:00

pages

123-9

issue

1-2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(15)00961-4

journal_volume

463

pub_type

杂志文章

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