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Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells

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Title: Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells
Authors: Zhang, Tao Browse this author
Zhao, Guannan Browse this author
Yang, Chuanhe Browse this author
Dong, Peixin Browse this author →KAKEN DB
Watari, Hidemichi Browse this author →KAKEN DB
Zeng, Lin Browse this author
Pfeffer, Lawrence M. Browse this author
Yue, Junming Browse this author
Keywords: ovarian cancer
epithelial to mesenchymal transition
Issue Date: Apr-2018
Publisher: Spandidos Publications
Journal Title: Oncology Letters
Volume: 15
Issue: 4
Start Page: 4432
End Page: 4438
Publisher DOI: 10.3892/ol.2018.7834
Abstract: Ovarian cancer is one of the most common malignancies in women and has a high mortality rate due to metastatic progression and tumor recurrence. ASAP1 (ArfGAP with SH3 Domain, Ankyrin Repeat and PH Domain 1) is an ADP-ribosylation factor GTPase-activating protein, which is involved in tumor metastasis. However, the role of ASAP1 in ovarian cancer is completely unknown. The present study reported that ASAP1 was highly expressed in ovarian carcinoma, and expression positively-correlated with overall poor survival and prognosis of patients. Lentiviral vector mediated ASAP1 expression promoted cell migration and invasion in ovarian cancer cell lines SKOV3 and OVCAR3. In addition, ASAP1 promoted cell proliferation, survival and inhibited chemotherapy drug paclitaxel-induced cell apoptosis. Furthermore, ASAP1 expression promoted epithelial to mesenchymal transition (EMT) by upregulating the mesenchymal cell markers N-cadherin and vimentin, and downregulating epithelial cell marker E-cadherin in the ovarian cancer cell lines. The data indicate for the first time that ASAP1 exhibits an oncogenic role by promoting EMT in ovarian cancer cells.
Type: article
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)

Submitter: 董 培新

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