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The Effect of Napsin A Gene on the Proliferation in Ephethlial-Mesenchymal Transition of Cell A549 and Its Mechanism
Shu-Hong Guan1, Jin-Xu Zheng2*, Qing Xu2, Yan Tang2, Ji-Zhu Liu2, Xiao-Ting Lü2
1School of Medical Science and Laboratory Medicine, Jiangsu University, Zhenjiang 212013, China; 2Department of Respiration, the Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China
Abstract: A recombinant lentiviral plasmid PLJM1-Napsin A was constructed and transfected into lung adenocarcinoma cell A549. Western blot assay was used to identify the stable expression of Napsin A protein. Ephethlial-mesenchymal transition model was established in vitro by the A549 cells treated with transforming growth factor beta-1. The cell proliferation was detected by MTT assay. The alteration of cell cycle were determined by flow cytometry. Then the expression of focal adhesion kinase were determined by Western blot. This study was to investigate the effect of Napsin A gene on the proliferation in ephethlial-mesenchymal transition of cell A549 and its mechanism. In vitro experiment showed A549 cell line with Napsin A gene infection was constructed successfully and Napsin A protein was expressed stably (P<0.01). Transforming growth factor beta-1 induced ephethlial-mesenchymal transition in A549 cells， as demonstrated by significant reduction of E-cadherin (P<0.01) as well as upregulation of collagen type I (P<0.01). Also transforming growth factor beta-1-inuced cell proliferation was inhibited by Napsin A (P<0.05). Further study demonstrated that Napsin A can cause G0/G1 arrest (P<0.01)and inhibit expression of focal adhesion kinase (P<0.01)， a key protein in integrin signaling pathway， in vitro ephethlial-mesenchymal transition model. Sustained Napsin A expression in A549 cells can inhibit the ephethlial-mesenchymal transition- induced proliferation. This may be due to blocked integrin signaling pathway by Napsin A.
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