Dingsheng Liu

Dingsheng Liu


Research Focus & Metrics

Academic Career Length

6Years (2021-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
19 September 2022 in Hematology
Verified
Journal Article
Open access
XZXiaojia Zuo
Xiaojia Zuo
DLDingsheng Liu
Dingsheng Liu
The mechanism of immunomodulatory drugs (IMiDs) resistance to multiple myeloma (MM) cells has been gradually demonstrated by recently studies, and some potential novel strategies have been confirme...

4 January 2021 in Journal of Hematopathology
Verified
Journal Article
Closed access
PDF file
XZXiaojia Zuo
Xiaojia Zuo
DLDingsheng Liu
Dingsheng Liu

2 October 2021 in Journal of Hematopathology
Verified
Journal Article
Closed access
PDF file
XZXiaojia Zuo
Xiaojia Zuo
JFJinyi Feng
Jinyi Feng
LYLilin Ye
Lilin Ye
MXMiao Xing
Miao Xing
ZDZhikui Deng
Zhikui Deng
DLDingsheng Liu
Dingsheng Liu

14 October 2022 in Journal of Oncology
Verified
Journal Article
Open access
PDF file
XZXiaojia Zuo
Xiaojia Zuo
CLChaojun Lu
Chaojun Lu
YZYanjun Zheng
Yanjun Zheng
DLDonglin Lai
Donglin Lai
DLDingsheng Liu
Dingsheng Liu
XGXuefeng Gu
Xuefeng Gu
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.