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PLAUR Confers Resistance to Gefitinib Through EGFR/P-AKT/Survivin Signaling Pathway
Author(s) -
Jian Zhou,
Kwang Joo Kwak,
Zuoren Wu,
Dawei Yang,
Jing Li,
Meijia Chang,
Yuanlin Song,
Hengshan Zeng,
L. James Lee,
Jie Hu,
Chunxue Bai
Publication year - 2018
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000491071
Subject(s) - gefitinib , biology , gene knockdown , cancer research , oncogene , cell cycle , rna interference , epidermal growth factor receptor , cell , apoptosis , cancer , rna , gene , biochemistry , genetics
Tyrosine kinase inhibitor gefitinib significantly improves the survival of patients with non-small-cell lung cancer (NSCLC) by inhibiting epidermal growth factor receptor (EGFR) tyrosine kinase. However, patients eventually develop resistance to gefitinib through uncharacterized mechanisms. It is known that plasminogen activator urokinase receptor (PLAUR) plays an important role in cell proliferation, migration and apoptosis. However, the role of PLAUR, particularly exosomal PLAUR in gefitinib resistance in NSCLC has not been reported. The aim of this study is to determine the relationship between PLAUR and gefitinib resistance.

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