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Study of NID1-promoted Migration and Invasion and Its Molecular Mechanism in Ovarian Cancer Cell OVCAR-3
Zhu Yuanyuan1,2, Zhang Chundong1,2, Wang Yitao1,2, Wang Sen1,2, Zhu Huifang1,2, Li Yi1,2, Lei Yunlong1,2, Bu Youquan1,2, Zhang Ying1,2*
1Department of Biochemistry and Molecular Biology, Chongqing Medical University, Chongqing 400016, China; 2Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China
Abstract: Nidogen-1 (NID1) is found to be a novel candidate diagnostic biomarker of ovarian cancer in our previous study， but its role in the development of ovarian cancer is unclear. In this study， we firstly established the OVCAR-3 monoclone with stable ectopic expression of NID1， and then assessed its migratory and invasive abilities by wound healing assay， Transwell migration and invasion assays. Subsequently， we utilized quantitative RT-PCR and Western blot to detect proteins relating to epithelial-mesenchymal transition (EMT) and ERK/MAPK signaling pathway in the NID1-overexpressed OVCAR-3 cells. The results showed that NID1-overexpressed OVCAR-3 cells exhibited significantly greater motility and invasiveness comparing with those of the control group; NID1 overexpression also led to the enhanced EMT phenotype， including the fibroblastic morphology， the reduction of the epithelial marker E-cadherin， the enhancement of mesenchymal markers (Vimentin and N-cadherin) and the transcription factor Twist-2. Furthermore， the levels of phosphorylated ERK1/2 were increased in NID1- overexpressed OVCAR-3 cells. After decreasing the ERK1/2 phosphorylation in these cells treated with an MEK inhibitor， U0126， the expressions of EMT relevant marks were regressed. Taken together， our findings reveal that NID1 promotes ovarian cancer metastasis， probably through the activation of the ERK/MAPK signaling pathway to propel EMT.
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