EFEMP1 promotes ovarian cancer cell growth, invasion and metastasis via activated the AKT pathway.

作者: Xiuxiu Yin , Shuang Fang , Mei Wang , Qiang Wang , Rui Fang

DOI: 10.18632/ONCOTARGET.10296

关键词: ImmunologyOvarian cancerCell cycle checkpointPI3K/AKT/mTOR pathwayMicroarray analysis techniquesCancer researchCarcinomaCell growthAkt/PKB signaling pathwayMetastasisMedicine

摘要: // Xiuxiu Yin 1, 2 , Shuang Fang 3 Mei Wang 4 Qiang 5 Rui 6 Jie Chen 1 Department of Maternal and Child Health, School Public Shandong University, Jinan, 250012, China The No.1 People’s Hospital Jining, Jining 272000, Biochemistry Molecular Biology, Georgetown Georgetown, Washington D.C, 20057, USA Pharmacy Department, Provincial affiliated to Obstetrics Gynecology, the Second Jilin Jilin, 130000, Clinical Medicine, Jinan Correspondence to: Chen, email: 77chenjie@sdu.edu.cn Keywords: EFEMP1, ovarian cancer, invasion, metastasis, EMT Received: March 14, 2016      Accepted: June 09, Published: 25, 2016 ABSTRACT a kind extracellular matrix (ECM) protein, has been suggested correlate with development different types carcinoma. However, its functions in cancer remain unclear. In our study, we performed cDNA microarray analysis identified EFEMP1 dramatically elevated highly invasive subclone, compared low subclone. Lentivirus transfection experiments were constructed afterwards. results demonstrated that knockdown significantly inhibited cell proliferation induced cycle arrest at G1/G0 phase. We also found decreased activity phospho-AKT could suppress invasion metastasis. Meanwhile, increased by overexpression had enhanced abilities cells invade migrate. addition, vivo nude mice model confirmed was tightly correlated tumor. RT Profiler PCR array further indicated suppressed epithelial-to-mesenchymal transition (EMT). Collectively, activating AKT signaling pathway, contributed metastasis as positive regulator. Overall, showed potential use new therapeutic strategies for cancer.

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