Evidence map›Paper›PMID 32275843›Full record

ArticleCell cycle (Georgetown, Tex.)2020

CDK1-PLK1/SGOL2/ANLN pathway mediating abnormal cell division in cell cycle may be a critical process in hepatocellular carcinoma.

Ling Li, Kang Huang, Huijia Zhao, Binyao Chen, Qifa Ye, Jiang Yue

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

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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

6 authors at 3 institutions in 1 country.

Ling LiZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, Hubei, RP China.
Kang HuangZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, Hubei, RP China.
Huijia ZhaoZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, Hubei, RP China.
Binyao ChenZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, Hubei, RP China.
Qifa YeZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, Hubei, RP China.
Jiang YueDepartment of Pharmacology, Basic Medical School of Wuhan University, Wuhan, Hubei, RP China.
Zhongnan Hospital of Wuhan University · CNWuhan University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aims to investigate the potential mechanisms and identify core biomarkers of Hepatocellular carcinoma (HCC). The profile GSE113850 was downloaded to analyze the differentially expressed genes. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction network analysis were used to reveal the main signal pathways of the differentially expressed genes (DEGs) and hub genes. The correlation between core gene expression and pathological stages, the disease-free survival analysis, the overall survival analysis were analyzed by Gene Expression Profiling Interactive Analysis. Furthermore, we reidentified the expression level of core genes of carcinoma tissues and para-carcinoma tissues from 14 HCC patients with real-time reverse transcription-polymerase chain reaction analysis (RT-PCR) and western blotting. After SK-Hep1 cell was treated with cyclin-dependent kinase 1 (CDK1) siRNA for 72 h, we detected the expression of the core genes and fluorescence-activated cell sorting analysis. A total of 378 DEGs were found. GO and KEGG analysis revealed that the DEGs were mainly enriched in the cell cycle. There were positive correlations among CDK1, polo-like kinase 1, shugoshin2 and anillin actin-binding protein. Moreover, the expression levels of four core genes were related to the HCC occurrence, pathological stages, and survivorship curve. The clinical HCC specimens verified the higher expression level of core genes by real-time RT-PCR. The transfection of siCDK1 in SK-Hep1 resulted in a disordered cell cycle. Furthermore, CDK1 knockdown suppressed the expression of PLK1, ANLN, and SGOL2. The CDK1-PLK1/SGOL2/ANLN pathway mediating abnormal cell division in the cell cycle might be a critical process in HCC.

Indexed as

Biomarkers, TumorCarcinoma, HepatocellularCDC2 Protein KinaseCell Cycle ProteinsCell DivisionCell Line, TumorComputational BiologyDisease-Free SurvivalGene Expression Regulation, NeoplasticGene OntologyGene Regulatory NetworksHumansLiver NeoplasmsMicrofilament ProteinsPolo-Like Kinase 1Protein Interaction MapsANLN protein, humanBiomarkers, TumorCDC2 Protein KinaseCDK1 protein, humanCell Cycle ProteinsMicrofilament ProteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsRNA, MessengerSGO2 protein, humanANLNbioinformaticsCDK1Hepatocellular carcinomaPLK1SGOL2

Identifiers

PMID32275843
PMCPMC7217380
OpenAlexW3016200455

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.