@Article{096504017X15112639918174,
AUTHOR = {Yi Long Wan, Han Jue Dai, Wei Liu, Hai Tao Ma},
TITLE = {miR-767-3p Inhibits Growth and Migration of Lung Adenocarcinoma  Cells by Regulating CLDN18},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {4},
PAGES = {637--644},
URL = {http://www.techscience.com/or/v26n4/56676},
ISSN = {1555-3906},
ABSTRACT = {Claudin18 (CLDN18) is necessary for intercellular junctions and is reported to be involved in cell migration and 
metastasis, making it like an oncogene in various cancer types. However, the biological function and regulatory 
mechanisms of CLDN18 in lung adenocarcinoma are not yet clear. In this study, we found downregulation of 
miR-767-3p and upregulation of CLDN18 in lung adenocarcinoma tissue and cell lines. In addition, there was 
a negative correlation between the expression of miR-767-3p and CLDN18 in lung adenocarcinoma. Double 
luciferase reporter gene analysis showed that miR-767-3p modulates the expression of CLDN18 by binding its 
3'-untranslated regions (3'-UTR). Knockdown of CLDN18 results in a decrease in the growth, migration, and 
invasion of lung adenocarcinoma cells. Although overexpression of miR-767-3p inhibits lung adenocarcinoma 
cell growth and migration, these effects can be rescued by reexpressing CLDN18. In summary, the data suggest 
that miR-767-3p inhibits tumor cell proliferation, migration, and invasion by targeting CLDN18, providing a 
promising therapeutic target for lung adenocarcinoma.},
DOI = {10.3727/096504017X15112639918174}
}