title: 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.
authors.affiliation: The Key Laboratory of Geriatrics, Beijing Hospital & Beijing Institute of Geriatrics, Ministry of Health, Beijing, China; Department of Biochemistry, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Electronic address: juzi.cui@gmail.com.
authors.forename: Ju
authors.initials: J
authors.lastname: Cui
authors.affiliation: Department of Biochemistry, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
authors.forename: Guoxiang
authors.initials: G
authors.lastname: Jin
authors.affiliation: Department of Biochemistry, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
authors.forename: Bin
authors.initials: B
authors.lastname: Yu
authors.affiliation: Department of Biochemistry, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China; Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China.
authors.forename: Zai
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Biochemistry, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
authors.forename: Raozhou
authors.initials: R
authors.lastname: Lin
authors.affiliation: Department of Biochemistry, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China; The Centre for Synthetic Biology Engineering Research, Shenzhen Institutes of Advanced Technology, Shenzhen, China. Electronic address: jdhuang@hku.hk.
authors.forename: Jian-Dong
authors.initials: JD
authors.lastname: Huang
mesh_terms: D000818:Animals; D015820:Cadherins / Q000378:metabolism; D002453:Cell Cycle; D002460:Cell Line; D016764:Cell Polarity / Q000235:genetics / Q000502:physiology; D049109:Cell Proliferation; D004285:Dogs; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics / Q000502:physiology*; D055785:Gene Knockdown Techniques; D006801:Humans; D016547:Kinesins / Q000037:antagonists & inhibitors / Q000172:deficiency* / Q000235:genetics; D061985:Madin Darby Canine Kidney Cells; D051379:Mice; D008819:Mice, Nude; D018995:Myosin Heavy Chains / Q000378:metabolism; D009362:Neoplasm Metastasis
chemical_list: D015820:Cadherins; D018995:Myosin Heavy Chains; D016547:Kinesins
keywords: Epithelial–mesenchymal transtion; Kif5b; MDCK cell