Oncotarget

Research Papers:

The inhibition of cordycepin on cancer stemness in TGF-beta induced chemo-resistant ovarian cancer cell

Chia-Woei Wang, Bao-Hong Lee and Chen-Jei Tai _

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Oncotarget. 2017; 8:111912-111921. https://doi.org/10.18632/oncotarget.22951

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Abstract

Chia-Woei Wang1,2, Bao-Hong Lee3,4 and Chen-Jei Tai1,2,3,4

1Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei 11042, Taiwan

2Department of Obstetrics and Gynecology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11042, Taiwan

3Department of Traditional Chinese Medicine, Department of Internal Medicine, Taipei Medical University Hospital, Taipei 11042, Taiwan

4Traditional Herbal Medicine Research Center, Taipei Medical University Hospital, Taipei 11042, Taiwan

Correspondence to:

Chen-Jei Tai, email: [email protected]

Keywords: cancer stem cells; chemotherapy; chemoresistance; cordycepin; ovarian cancer

Received: August 31, 2017     Accepted: November 15, 2017     Published: December 05, 2017

ABSTRACT

Chemotherapy is one of the main approach for ovarian cancer. Cancer stem cells (CSCs) escape chemotherapy and lead to chemoresistance. We previously demonstrated that cordycepin (Cd) inhibited metastasis in human ovarian carcinoma cells, the aim of this study is to investigate the effects of Cd on ovarian cancer stemness. TGF-beta was used to induce chemoresistance of chemotherapeutic agent cisplatin in SKOV-3 ovarian cancer cells. After treating with 100 μM of Cd, cell viability, the percentage of cancer stem cells, and the levels of matrix metalloproteinases (MMPs) were decreased in TGF-beta-induced SKOV-3 cells. Treatment of Cd recovered E-cadherin levels and inhibited vimentin levels while TGF-beta treatment significantly increased the expression of vimentin and PGC-1alpha, and decreased E-cadherin levels in SKOV-3 cells, indicating that the action of Cd on cancer stemness may contribute to the regulation of epithelial-mesenchymal transition (EMT). Cd efficiently attenuated chemoresistance caused by TGF-beta in SKOV-3 cancer stem cells to promote the cytotoxicity of cisplatin.


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