Evidence map›Paper›PMID 31703591›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Upregulation of CENPM promotes hepatocarcinogenesis through mutiple mechanisms.

Yusha Xiao, Rahmathullah Mohamed Najeeb, Dong Ma, Kang Yang, Qiu Zhong, Quanyan Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

59 citing papers in PubMed, 75 citations in OpenAlex.

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  14. [Circ_0026134 regulates the miR-1270/GRB2 pathway to affect the radiosensitivity of hepatoma cells].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024
    Article
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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 1 institution in 1 country.

Yusha XiaoDepartment of General Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei, People's Republic of China.
Rahmathullah Mohamed NajeebDepartment of General Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei, People's Republic of China.
Dong MaDepartment of General Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei, People's Republic of China.
Kang YangDepartment of Urology, Renmin Hospital of Wuhan University, Hubei, China.
Qiu ZhongDepartment of General Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei, People's Republic of China.
Quanyan LiuDepartment of General Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei, People's Republic of China. lqy@whu.edu.cn.ORCID http://orcid.org/0000-0002-5353-0377
Wuhan University · CN

Funding

National Natural Science Foundation of China 81872029, 81572450
6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) still remains a dominating medical challenge in early diagnosis and clinical therapy. Centromere protein M (CENPM) has been proved to be over-expressed in HCC tissues, but carcinogenic mechanism of CENPM contributing to liver cancer is poorly understood.

methodsIn this study, we first explored mRNA and protein levels of CENPM in HCC samples, matching adjacent non-tumor tissues and six hepatoma cell lines by polymerase chain reaction (PCR), western blotting and immunohistochemistry (IHC). Clinical data of HCC patients downloaded from The Cancer Genome Atlas (TCGA) were also analyzed. The character of CENPM concerned with HCC progression through several functional experimentations in vitro and in vivo was researched. Bioinformatics was carried out to further discover biological functions of CENPM.

resultsCENPM was positively up-regulated in HCC and connected with a poor prognosis. Silencing CENPM repressed cell proliferation in vivo and in vitro, and knock-down CENPM inhibited cell migration and invasion. Additionally, depletion of CENPM can promote cell apoptosis and arrested cell cycle. Furthermore, single-gene gene set enrichment analysis (GSEA) analysis indicated that CENPM was linked to the P53 signaling pathway and cell cycle pathway, and our research supported this prediction. Finally, we also found that miR-1270 was a negative regulator and participated in post-transcriptional regulation of CENPM, and hepatitis B virus X protein (HBx) can promote hepatocellular carcinoma by suppressing miR1270.

conclusionCENPM was closely associated with HCC progression and it could be considered as a new possible biomarker along with a therapeutic target for HCC.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinoma, HepatocellularCell CycleCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticChromosomal Proteins, Non-HistoneComputational BiologyDisease Models, AnimalFemaleGene Expression ProfilingHumansKaplan-Meier EstimateLiver NeoplasmsChromosomal Proteins, Non-HistoneBioinformaticsCentromere protein M (CENPM)Hepatocellular carcinoma (HCC)miR-1270P53The Cancer genome atlas (TCGA)

Identifiers

PMID31703591
PMCPMC6839178
OpenAlexW2983428551

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.