Open AccessERGIC 3, which is regulated by miR‐203a, is a potential biomarker for non‐small cell lung cancer
Author(s) -
Lin QingHai,
Zhang KuiDong,
Duan HeXian,
Liu MinXia,
Wei WanLi,
Cao Yi
Publication year - 2015
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12741
Subject(s) - immunohistochemistry , pathology , biology , monoclonal antibody , lung cancer , epithelium , cancer research , in vivo , antibody , cancer , transfection , lung , downregulation and upregulation , cell culture , medicine , immunology , gene , biochemistry , genetics , microbiology and biotechnology
In a previous study, we found that ERGIC 3 was a novel lung cancer‐related gene by screening libraries of differentially expressed genes. In this study, we developed a new murine monoclonal antibody ( mA b) against ERGIC 3. This avid antibody (6‐C4) is well suited for immunohistochemistry, immunoblotting and solid‐phase immunoassays. Furthermore, we systematically investigated expressions of ERGIC 3 in a broad variety of normal human tissues and various types of tumors by immunohistochemistry. In normal human tissues, 6‐C4 reacted only in some epithelial cells, such as hepatocytes, gastrointestinal epithelium, ducts and acini of the pancreas, proximal and distal tubules of the kidney, and mammary epithelial cells; however, most normal human tissues were not stained. Moreover, almost all carcinomas that originated from the epithelial cells were positive for 6‐C4, whereas all sarcomas were negative. Notably, 6‐C4 strongly stained non‐small cell lung cancer ( NSCLC ) cells but did not react with normal lung tissues. Hence, ERGIC3 mAb could be used in histopathological diagnosis and cytopathological testing to detect early‐stage NSCLC . We also studied the mechanisms of ERGIC 3 regulation in vitro and in vivo by means of bioinformatics analysis, luciferase reporter assay, mi RNA expression profiling and mi RNA transfection. Results showed that miR‐203a downregulation induced ERGIC 3 overexpression in NSCLC cells.