Oncotarget

Research Papers:

XB130 translocation to microfilamentous structures mediates NNK-induced migration of human bronchial epithelial cells

Qifei Wu _, Jeya Nadesalingam, Serisha Moodley, Xiaohui Bai and Mingyao Liu

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Oncotarget. 2015; 6:18050-18065. https://doi.org/10.18632/oncotarget.3777

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Abstract

Qifei Wu1,2,*, Jeya Nadesalingam1,*, Serisha Moodley1,3, Xiaohui Bai1, Mingyao Liu1,3,4

1Latner Thoracic Surgery Research Laboratories, University Health Network, Toronto General Research Institute, Toronto, Ontario, Canada

2Department of Thoracic Surgery, The First Affiliated Hospital, School of Medicine, Xi’an Jiaotong University, Xi’an, China

3Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada

4Department of Surgery, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada

*These authors have contributed equally to this work

Correspondence to:

Mingyao Liu, e-mail: mingyao.liu@utoronto.ca

Keywords: airway epithelial cell migration, F-actin association, cortactin, intracellular signal transduction

Received: December 18, 2014     Accepted: April 09, 2015     Published: April 20, 2015

ABSTRACT

Cigarette smoking contributes to the pathogenesis of chronic obstructive pulmonary disease and lung cancer. Nicotine-derived nitrosamine ketone (NNK) is the most potent carcinogen among cigarette smoking components, and is known to enhance migration of cancer cells. However, the effect of NNK on normal human bronchial epithelial cells is not well studied. XB130 is a member of actin filament associated protein family and is involved in cell morphology changes, cytoskeletal rearrangement and outgrowth formation, as well as cell migration. We hypothesized that XB130 mediates NNK-induced migration of normal human bronchial epithelial cells. Our results showed that, after NNK stimulation, XB130 was translocated to the cell periphery and enriched in cell motility-associated structures, such as lamellipodia, in normal human bronchial epithelial BEAS2B cells. Moreover, overexpression of XB130 significantly enhanced NNK-induced migration, which requires both the N- and C-termini of XB130. Overexpression of XB130 enhanced NNK-induced protein tyrosine phosphorylation and promoted matrix metalloproteinase-14 translocation to cell motility-associated cellular structures after NNK stimulation. XB130-mediated NNK-induced cell migration may contribute to airway epithelial repair; however, it may also be involved in cigarette smoking-related chronic obstructive pulmonary disease and lung cancer.


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