Open AccessNID1, a new regulator of EMT required for metastasis and chemoresistance of ovarian cancer cells
Author(s) -
Ya Zhou,
Yuanyuan Zhu,
Xiaoyan Fan,
Chun-Dong Zhang,
Ying Wang,
Lian Zhang,
Huan Zhang,
Tao Wen,
Kaina Zhang,
Xiao Huo,
Xue Jiang,
Youquan Bu,
Ying Zhang
Publication year - 2017
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.16145
Subject(s) - ovarian cancer , cancer research , metastasis , epithelial–mesenchymal transition , gene knockdown , ectopic expression , motility , cisplatin , cancer , phenotype , mapk/erk pathway , medicine , biology , signal transduction , apoptosis , cell culture , gene , microbiology and biotechnology , chemotherapy , genetics
Nidogen-1 (NID1) has been identified as a novel candidate diagnostic biomarker of ovarian cancer in our previous study. Nevertheless, the role of NID1 in the pathogenesis of ovarian cancer is unclear. In the present study, we demonstrated that NID1 was a mesenchymal associated gene and its high expression was significantly correlated with shorter overall survival of ovarian cancer patients. The ectopic expression of NID1 in OVCAR-3 cells revealed a epithelial-mesenchymal transition (EMT) phenotype accompanied by enhancement of motility, invasiveness and cisplatin resistance, whereas the knockdown of NID1 was sufficient to convert HEY cells into epithelial phenotype with decreased capability of motility, invasiveness and cisplatin resistance. Mechanistic studies disclosed that NID1 activated ERK/MAPK signaling pathway to promote EMT. Collectively, our findings have uncovered the molecular mechanisms of NID1 in promoting ovarian cancer metastasis and chemoresistance, and provide a rationale for the therapeutic potential of NID1 suppression in ovarian cancer.