Effects of the Targeted Regulation of CCRK by miR-335-5p on the Proliferation and Tumorigenicity of Human Renal Carcinoma Cells

Xiaojia Zuo; Chaojun Lu; Yanjun Zheng; Donglin Lai; Dingsheng Liu; Guoqing Wan; Changlian Lu; Xuefeng Gu

doi:10.1155/2022/2960050

Effects of the Targeted Regulation of CCRK by miR-335-5p on the Proliferation and Tumorigenicity of Human Renal Carcinoma Cells

J Oncol. 2022 Oct 14:2022:2960050. doi: 10.1155/2022/2960050. eCollection 2022.

Authors

Xiaojia Zuo^{1

2

3}, Chaojun Lu⁴, Yanjun Zheng¹, Donglin Lai^{1

5}, Dingsheng Liu¹, Guoqing Wan¹, Changlian Lu¹, Xuefeng Gu^{1

5

6}

Affiliations

¹ Shanghai Key Laboratory of Molecular Imaging, Zhoupu Hospital, Shanghai University of Medicine and Health Science, Shanghai, China.
² Shanghai Gongli Hospital, The Second Military Medical University, Shanghai, China.
³ School of Medical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.
⁴ Operation Room, Huashan Hospital Affiliated to Fudan University, Shanghai, China.
⁵ School of Medical Instruments and Food Engineering, University of Shanghai for Science and Technology, Shanghai, China.
⁶ School of Pharmacy, Shanghai University of Medicine and Health Sciences, Shanghai, China.

Abstract

Cell cycle-related kinase (CCRK) is most closely related to cyclin-dependent protein kinase, which may activate cyclin-dependent kinase 2 and is associated with the growth of human cancer cells. However, the expression and function of CCRK in the pathogenesis of clear cell renal cell cancer (ccRCC) are unclear. Herein, this research aimed to explore the potential mechanism of the targeted regulation of CCRK by miR-335-5p on the proliferation and tumorigenicity of human ccRCC cells. The results showed that CCRK was significantly overexpressed in ccRCC tissues and cells, and knockdown of the CCRK expression by shRNA inhibited cell proliferation in vitro and in vivo and enhanced cell apoptosis in vitro, which indicated that CCRK could be a potential target for antitumour drugs in the treatment of ccRCC. Moreover, miR-335-5p was found to bind directly to the 3' untranslated region of CCRK, was expressed at markedly low levels in ccRCC cells, and was closely associated with the tumour stage. The overexpression of CCRK partially reversed the inhibitory effects of miR-335-5p on the cell growth of ccRCC, which implied that miR-335-5p could serve as a promising tumour inhibitor for ccRCC. In summary, CCRK could serve as an alternative antitumour drug target, and miR-335-5p could be a promising therapeutic tumour inhibitor for ccRCC treatment.