期刊
INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
卷 27, 期 4, 页码 628-633出版社
BMJ PUBLISHING GROUP
DOI: 10.1097/IGC.0000000000000928
关键词
Cervical cancer; Kin17; Proliferation; Invasion; Apoptosis
资金
- National Natural Science Foundation of PR China [81201831]
- Guangdong Planning Project of Science and Technology [2016A020215118]
- Social Science and Technology Development Program of Dongguan [2013108101061]
- Dongguan Science and Technology Planning Project of Medical Treatment and Public Health [20131051010005]
Background Cervical cancer is one of the most common cancers in women worldwide. Emerging evidence suggests that kin17 is a tumor-promoting protein in some types of solid tumors. However, whether kin17 contributes to cervical cancer carcinogenesis remains unknown. Methods Kin17 expression in clinical samples from Guangdong Women and Children's Hospital and Health Institute was detected by immunohistochemical staining. A series of functional experiments including 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, 5-bromo-2-deoxyuridine assay, colony formation, transwell assay, flow cytometry of apoptosis, and cell cycle were performed to explore the roles of kin17 in cervical cancer cells HeLa. Results In this study, we showed for the first time that the expression of kin17 was significantly increased in clinical cervical cancer samples, and associated with tumor differentiation, lymph node metastasis, and ki-67 expression in a clinicopathologic characteristics review. Furthermore, silence of kin17 in HeLa cells inhibited cell proliferation, clone formation, cell cycle progression, migration, and invasion, and also promoted cell apoptosis. Conclusion Our findings demonstrate that kin17 is closely related to the cell proliferation and invasion of cervical cancer and could be a novel diagnostic and therapeutic target for cervical cancer management. The underlying mechanisms should be elucidated in future research.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据