title: EFEMP1 promotes ovarian cancer cell growth, invasion and metastasis via activated the AKT pathway.
abstract: EFEMP1, a kind of extracellular matrix (ECM) protein, has been suggested to correlate with the development of different types of carcinoma. However, its functions in ovarian cancer remain unclear. In our study, we performed cDNA microarray analysis and identified EFEMP1 dramatically elevated in the highly invasive subclone, compared with the low invasive subclone. Lentivirus transfection experiments were constructed afterwards. The results demonstrated that knockdown of EFEMP1 significantly inhibited ovarian cancer cell proliferation and induced cell cycle arrest at the G1/G0 phase. We also found that decreased the activity of phospho-AKT could suppress cell invasion and metastasis. Meanwhile, the increased phospho-AKT activity induced by the overexpression of EFEMP1 had significantly enhanced the abilities of ovarian cancer cells to invade and migrate. In addition, the vivo nude mice model confirmed that EFEMP1 was tightly correlated with the development of tumor. The results of RT2 Profiler EMT PCR array further indicated that decreased EFEMP1 suppressed epithelial-to-mesenchymal transition (EMT). Collectively, by activating AKT signaling pathway, EFEMP1 contributed to ovarian cancer invasion and metastasis as a positive regulator. Overall, EFEMP1 had showed the potential use in the development of new therapeutic strategies for ovarian cancer.
authors.affiliation: Department of Maternal and Child Health, School of Public Health, Shandong University, Jinan, 250012, China.|The No.1 People's Hospital of Jining, Jining 272000, China.
authors.forename: Xiuxiu
authors.initials: X
authors.lastname: Yin
authors.affiliation: Biochemistry and Molecular Biology, Georgetown University, Georgetown, Washington D.C, 20057, USA.
authors.forename: Shuang
authors.initials: S
authors.lastname: Fang
authors.affiliation: Pharmacy Department, Shandong Provincial Hospital affiliated to Shandong University, Jinan, 250012, China.
authors.forename: Mei
authors.initials: M
authors.lastname: Wang
authors.affiliation: Department of Obstetrics and Gynecology, the Second Hospital affiliated to Jilin University, Jilin, 130000, China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Wang
authors.affiliation: Clinical Medicine, School of Medicine, Shandong University, Jinan 250012, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Fang
authors.affiliation: Department of Maternal and Child Health, School of Public Health, Shandong University, Jinan, 250012, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
mesh_terms: D000818:Animals; D059447:Cell Cycle Checkpoints / Q000502:physiology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000502:physiology; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D005260:Female; D064593:Heterografts; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D051058:Oncogene Protein v-akt / Q000378:metabolism*; D010051:Ovarian Neoplasms / Q000378:metabolism* / Q000473:pathology*; D015398:Signal Transduction; D014162:Transfection
chemical_list: C119630:EFEMP1 protein, human; D016326:Extracellular Matrix Proteins; D051058:Oncogene Protein v-akt
keywords: EFEMP1; EMT; invasion; metastasis; ovarian cancer