MicroRNA-664 suppresses the growth of cervical cancer cells via targeting c-Kit
Authors Lv M, Ou R, Zhang Q, Lin F, Li X, Wang K, Xu Y
Received 29 January 2019
Accepted for publication 22 May 2019
Published 17 July 2019 Volume 2019:13 Pages 2371—2379
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Manfred Ogris
Mingfen Lv,1,2 Rongying Ou,3 Qianwen Zhang,1 Fan Lin,1 Xiangyun Li,4 Keyu Wang,2 Yunsheng Xu1,4
1Department of Dermatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, People’s Republic of China; 2Department of Dermatology, Qilu Hospital, Shandong University, Jinan, Shandong 250012, People’s Republic of China; 3Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, People’s Republic of China; 4Department of Dermatology, The Seventh Affiliated Hospital of Sun Yat-sen university, Shenzhen, Guangdong 518107, People’s Republic of China
Background: Cervical cancer is the second most common malignant cancer in women worldwide. Evidence indicated that miR-664 was significantly downregulated in cervical cancer. However, the mechanisms by which miR-664 regulates the tumorigenesis of cervical cancer remain unclear. Thus, this study aimed to investigate the role of miR-664 in cervical cancer.
Methods: Quantitative reverse transcription polymerase chain reaction was used to detect the level of miR-664 in tumor tissues and cell line. The dual luciferase reporter system assay and Western blotting were used to explore the interaction of miR-664 and c-Kit in cervical cancer.
Results: The expression of miR-664 in patients with cervical cancer was dramatically decreased compared with that in adjacent tissues. MiR-664 mimics significantly inhibited proliferation in SiHa cells via inducing apoptosis. In addition, miR-664 mimics induced apoptosis in SiHa cells via increasing the expressions of Bax and active caspase 3 and decreasing the level of Bcl-2. Moreover, dual-luciferase assay showed that c-Kit was the directly binding target of miR-664 in SiHa cells; overexpression of miR-664 downregulated the expression of c-Kit. Meanwhile, upregulation of miR-664 significantly decreased the levels of c-Myc and Cyclin D in cells. Furthermore, miR-664 markedly inhibited tumor growth of cervical cancer in xenograft.
Conclusion: Our data indicated that miR-664 exerted antitumor effects on SiHa cells by directly targeting c-Kit in vitro and in vivo. Therefore, miR-664 might be a potential therapeutic target for the treatment of patients with cervical cancer.
Keywords: microRNA-664, c-Kit, cervical cancer, apoptosis
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