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Elevated Expression of Kin17 in Cervical Cancer and Its Association With Cancer Cell Proliferation and Invasion
  1. Yuzhao Zhang, MS*,
  2. Hongyi Gao, MS,
  3. Xiang Gao, MS*,
  4. Senlin Huang, MS,
  5. Kunhe Wu, MS,
  6. Xiaobin Yu, MS*,
  7. Kaitao Yuan, PhD§ and
  8. Tao Zeng, PhD*,
  1. * Laboratory Medicine Center, Nanfang Hospital, Southern Medical University;
  2. Department of Pathology, Guangdong Women and Children Hospital;
  3. The First Clinical Medicine College, Southern Medical University;
  4. § Department of General Sugery, The First Affiliated Hospital, Sun Yet-sen University, Guangzhou; and
  5. School of Laboratory Medicine, Guangdong Medical University, Dongguan, PR China.
  1. Address correspondence and reprint requests to Tao Zeng, PhD, Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou Road North, Baiyun District, Guangzhou, PR China. E-mail: zengt{at}smu.edu.cn.

Abstract

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.

  • Cervical cancer
  • Kin17
  • Proliferation
  • Invasion
  • Apoptosis

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  • The authors declare no conflicts of interest.

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