@Article{096504017X15035795904677,
AUTHOR = {Changyu Liu, Yongde Liao, Sheng Fan, Xiangning Fu, Jing Xiong, Sheng Zhou, 
Man Zou, Jianmiao Wang},
TITLE = {G-Protein-Coupled Estrogen Receptor Antagonist G15 Decreases  Estrogen-Induced Development of Non-Small Cell Lung Cancer},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {3},
PAGES = {283--292},
URL = {http://www.techscience.com/or/v27n3/48590},
ISSN = {1555-3906},
ABSTRACT = {G-protein-coupled estrogen receptor (GPER) was found to promote non-small cell lung cancer (NSCLC) by 
estrogen, indicating the potential necessity of inhibiting GPER by a selective antagonist. This study was performed to elucidate the function of GPER-selective inhibitor G15 in NSCLC development. Cytoplasmic GPER 
(cGPER) and nuclear GPER (nGPER) were detected by immunohistochemical analysis in NSCLC samples. 
The relation of GPER and estrogen receptor (ER ) expression and correlation between GPER, ER , and 
clinical factors were analyzed. The effects of activating GPER and function of G15 were analyzed in the proliferation of A549 and H1793 cell lines and development of urethane-induced adenocarcinoma. Overexpression 
of cGPER and nGPER was detected in 80.49% (120/150) and 52.00% (78/150) of the NSCLC samples. High 
expression of GPER was related with higher stages, poorer differentiation, and high expression of ER . The 
protein level of GPER in the A549 and H1793 cell lines was increased by treatment with E2, G1 (GPER agonist), or fulvestrant (Ful; ER antagonist) and decreased by G15. Administration with G15 reversed the E2- or 
G1-induced cell growth by inhibiting GPER. In urethane-induced adenocarcinoma mice, the number of tumor 
nodules and tumor index increased in the E2 or G1 group and decreased by treatment with G15. These findings demonstrate that using G15 to block GPER signaling may be considered as a new therapeutic target in 
NSCLC.},
DOI = {10.3727/096504017X15035795904677}
}