Evidence map›Paper›PMID 30774374›Full record

ArticleOncoTargets and therapy2019

Downregulation of CENPK suppresses hepatocellular carcinoma malignant progression through regulating YAP1.

Jianlin Wang, Haimin Li, Congcong Xia, Xisheng Yang, Bin Dai, Kaishan Tao, Kefeng Dou

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-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

19 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  7. The cell cycle gene centromere protein K (Translational cancer research · 2022
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  17. High mRNA Expression ofDisease markers · 2021
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  19. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Jianlin WangDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China, doukef@fmmu.edu.cn; taokaishan0686@163.com.
Haimin LiDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China, doukef@fmmu.edu.cn; taokaishan0686@163.com.
Congcong XiaDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China, doukef@fmmu.edu.cn; taokaishan0686@163.com.
Xisheng YangDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China, doukef@fmmu.edu.cn; taokaishan0686@163.com.
Bin DaiDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China, doukef@fmmu.edu.cn; taokaishan0686@163.com.
Kaishan TaoDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China, doukef@fmmu.edu.cn; taokaishan0686@163.com.
Kefeng DouDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China, doukef@fmmu.edu.cn; taokaishan0686@163.com.
Air Force Medical University · CNSecond Military Medical University · CNEastern Hepatobiliary Surgery Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral studies have found that centromere protein K (CENPK) is overexpressed in several tumour types and promotes tumor progression. However, there has been little research on the role of CENPK in the progression of hepatocellular carcinoma (HCC). MATERIALS AND

methodsThe expression of CENPK in HCC tissues was quantified by Western blot and quantitative real-time PCR. Cells were transfected with lentiviral plasmids containing shRNA sequences targeting CENPK and YAP1 to silence the expression of CENPK and YAP1. Cell Counting Kit-8 assay, colony formation assay, wound healing assay, and transwell invasion assay were performed to evaluate cell growth, migration, and invasion of HCC cells. Tumorigenicity assay was used to detect the effect of CENPK on the growth of HCC cells. Western blot assay was performed to investigate the expression of epithelial-mesenchymal transition (EMT) markers and YAP1.

resultsCompared to that in adjacent non-tumor tissues, CENPK was aberrantly upregulated in HCC tumor tissues. Furthermore, CENPK knockdown significantly inhibited proliferation, migration, invasion, and EMT progression in HCC cells. Mechanistically, we identified that YAP1 was responsible for the tumor-suppressive effects of CENPK knockdown in the HCC cells. The inhibitory effects of CENPK silencing on cell proliferation, migration, invasion, and EMT were partially reversed by the restoration of YAP1 expression.

conclusionOur results suggested that the CENPK-YAP1-EMT axis plays a critical role in regulating HCC malignant progression, indicating the role of this axis as a potential therapeutic target for HCC.

Indexed as

CENPKEMTHCCmigration and invasionproliferationYAP1

Identifiers

PMID30774374
PMCPMC6357898
OpenAlexW2913054182

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.