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Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Medicine / Faculty of Medicine >
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Knockout of MTF1 Inhibits the Epithelial to Mesenchymal Transition in Ovarian Cancer Cells
This item is licensed under:Creative Commons Attribution-NonCommercial 4.0 International
| Title: | Knockout of MTF1 Inhibits the Epithelial to Mesenchymal Transition in Ovarian Cancer Cells |
| Authors: | Ji, Liang Browse this author | | Zhao, Guannan Browse this author | | Zhang, Peng Browse this author | | Huo, Wenying Browse this author | | Dong, Peixin Browse this author →KAKEN DB | | Watari, Hidemichi Browse this author →KAKEN DB | | Jia, Limin Browse this author | | Pfeffer, Lawrence M Browse this author | | Yue, Junming Browse this author | | Zheng, Jinhua Browse this author |
| Keywords: | MTF1 | | CRISPR/Cas9 nickase | | lentiviral vector | | ovarian cancer | | epithelial to mesenchymal transition |
| Issue Date: | 2018 |
| Publisher: | Ivyspring International Publisher |
| Journal Title: | Journal of Cancer |
| Volume: | 9 |
| Issue: | 24 |
| Start Page: | 4578 |
| End Page: | 4585 |
| Publisher DOI: | 10.7150/jca.28040 |
| Abstract: | Due to peritoneal metastasis and frequent recurrence, ovarian cancer has the highest mortality among gynecological cancers. Epithelial to mesenchymal transition (EMT) contributes to ovarian tumor metastasis. In this study, we report for the first time that metal regulatory transcription factor 1 (MTF1) was upregulated in ovarian cancer, and its high expression was associated with poor patient survival and disease relapse. Knockout of MTF1 using lentiviral CRISPR/Cas9 nickase vector-mediated gene editing inhibited EMT by upregulating epithelial cell markers E-cadherin and cytokeratin 7, and downregulating mesenchymal markers Snai2 and β-catenin in ovarian cancer SKOV3 and OVCAR3 cells. Loss of MTF1 reduced cell proliferation, migration, and invasion in both SKOV3 and OVCAR3 cells. Knockout of MTF1 upregulated the expression of the KLF4 transcription factor, and attenuated two cellular survival pathways, ERK1/2 and AKT. Our studies demonstrated that MTF1 plays an oncogenic role and contributes to ovarian tumor metastasis by promoting EMT. MTF1 may be a novel biomarker for early diagnosis as well as a drug target for clinical therapy. |
| Rights: | https://creativecommons.org/licenses/by-nc/4.0/ |
| Type: | article |
| URI: | http://hdl.handle.net/2115/72342 |
| Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 董 培新
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