Evidence map›Paper›PMID 29503564›Full record

ArticleOncoTargets and therapy2018

CDCA5 regulates proliferation in hepatocellular carcinoma and has potential as a negative prognostic marker.

Zhiqing Shen, Xueping Yu, Yijuan Zheng, Xueping Lai, Julan Li, Yuxiang Hong, Huatang Zhang, Chunlin Chen, Zhijun Su, Ruyi Guo

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.1field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 65 citations in OpenAlex.

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  20. Cyclin-Dependent Kinase 1 (CDK1) is Co-Expressed with CDCA5: Their Functions in Gastric Cancer Cell Line MGC-803.Medical science monitor : international medical journal of experimental and clinical research · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Zhiqing Shen *Department of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Xueping Yu *Department of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Yijuan ZhengDepartment of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Xueping LaiDepartment of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Julan LiDepartment of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Yuxiang HongDepartment of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Huatang ZhangDepartment of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Chunlin ChenDepartment of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Zhijun SuDepartment of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Ruyi GuoDepartment of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Fujian Medical University · CNOffice of Infectious Diseases · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCDCA5 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

methodsWe 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.

resultsIncreased 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.

conclusionThe present data warrant consideration of CDCA5 as a prognostic biomarker and therapeutic target for HCC.

Indexed as

apoptosisCDCA5cell cycleHCCproliferation

Identifiers

PMID29503564
PMCPMC5824752
OpenAlexW2789969476

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.