Open AccessOestrogen receptor‐mediated expression of Olfactomedin 4 regulates the progression of endometrial adenocarcinoma
Author(s) -
Duan Chao,
Liu Xubin,
Liang Shuang,
Yang Zheng,
Xia Meng,
Wang Liantang,
Chen Shangwu,
Yu Li
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12232
Subject(s) - adenocarcinoma , cancer research , endometrial cancer , progesterone receptor , endometrium , carcinoma , carcinogenesis , biology , medicine , oncology , cancer , estrogen receptor , breast cancer
Endometrial adenocarcinoma is the most common tumour of the female genital tract in developed countries, and oestrogen receptor ( ER ) signalling plays a pivotal role in its pathogenesis. When we used bioinformatics tools to search for the genes contributing to gynecological cancers, the expression of Olfactomedin 4 ( OLFM 4) was found by digital differential display to be associated with differentiation of endometrial adenocarcinoma. Aberrant expression of OLFM 4 has been primarily reported in tumours of the digestive system. The mechanism of OLFM 4 in tumuorigenesis is elusive. We investigated OLFM 4 expression in endometrium, analysed the association of OLFM 4 with ER signalling in endometrial adenocarcinoma, and examined the roles of OLFM 4 in endometrial adenocarcinoma. Expression of OLFM 4 was increased during endometrial carcinogenesis, linked to the differentiation of endometrioid adenocarcinoma, and positively related to the expression of oestrogen receptor‐α ( ER α) and progesterone receptor. Moreover, ER α‐mediated signalling regulated expression of OLFM 4, and knockdown of OLFM 4 enhanced proliferation, migration and invasion of endometrial carcinoma cells. Down‐regulation of OLFM 4 was associated with decreased cumulative survival rate of patients with endometrioid adenocarcinoma. Our data suggested that impairment of ER α signal‐mediated OLFM 4 expression promoted the malignant progression of endometrioid adenocarcinoma, which may have significance for the therapy of this carcinoma.