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Authors Shen Z, Yu X, Zheng Y, Lai X, Li J, Hong Y, Zhang H, Chen C, Su Z, Guo R
Received 21 October 2017
Accepted for publication 28 December 2017
Published 20 February 2018 Volume 2018:11 Pages 891—901
DOI https://doi.org/10.2147/OTT.S154754
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Manfred Beleut
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Geoffrey Pietersz
Background: CDCA5 plays an important role
in the development of various human cancers, but the associated mechanisms have
not been investigated in hepatocellular carcinoma (HCC).
Materials and methods: We evaluated expression levels and functions of
CDCA5 in HCC and showed that CDCA5 is upregulated in HCC tissues compared with
paired or unpaired normal liver tissues.
Results: Increased CDCA5 expression in HCCs was
significantly associated with shorter survival of patients. Knockdown of CDCA5
using lentivirus-mediated shRNA significantly inhibited cell proliferation and
suppressed cell survival, as well as induced cell cycle arrest at the G2/M
phase and cell apoptosis of HCC cells. The tumor suppression effects of CDCA5
knockdown were mediated by decreased expression of cyclin-dependent kinase 1
(CDK1) and CyclinB1, which were increased in HCC tissues comparing with
adjacent normal liver tissues. Moreover, upregulation of CDCA5 was positively
associated with increased CDK1 and CyclinB1 expression in HCC tissues.
Conclusion: The present data warrant consideration of CDCA5 as a
prognostic biomarker and therapeutic target for HCC.
Keywords: HCC, CDCA5,
proliferation, apoptosis, cell cycle