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Subcellular proteomics revealed the epithelial–mesenchymal transition phenotype in lung cancer
Author(s) -
Li LiPing,
Lu Chun Hua,
Chen ZhiPeng,
Ge Feng,
Wang Tong,
Wang Wei,
Xiao ChuanLe,
Yin XinFeng,
Liu Langxia,
He JianXing,
He QingYu
Publication year - 2011
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200900819
Subject(s) - epithelial–mesenchymal transition , proteomics , biology , carcinogenesis , a549 cell , phenotype , western blot , metastasis , cancer research , lung cancer , subcellular localization , gene silencing , tumor progression , cancer , pathology , microbiology and biotechnology , cell culture , medicine , gene , genetics , cytoplasm
Abstract Subcellular proteomics was used to compare the protein profiles between human lung adenocarcinoma A549 cells and human bronchial epithelial (HBE) cells. In total, 106 differential proteins were identified and the altered expression levels of partial identified proteins were confirmed by Western blot analysis. Importantly, pathway analysis and biological validation revealed epithelial–mesenchymal transition (EMT) phenotype shift in A549 cells as compared with HBE cells. The EMT phenotype of A549 cells can be increased by self‐producing TGF‐β1 and significantly decreased by silencing heterogeneous nuclear ribonucleoprotein (hnRNPK) expression. As EMT has been considered as an important event during malignant tumor progression and metastasis, investigating EMT and deciphering the related pathways may lead to more efficient strategies to fight lung cancer progression. By integrating the subcellular proteomic data with EMT‐related functional studies, we revealed new insights into the EMT progress of lung carcinogenesis, providing clues for further investigations on the discovery of potential therapeutic targets.