Evidence map›Paper›PMID 26442588›Full record

ArticleThe Journal of biological chemistry2015

Tumor Suppressive Function of p21-activated Kinase 6 in Hepatocellular Carcinoma.

Weisi Liu, Yidong Liu, Haiou Liu, Weijuan Zhang, Qiang Fu, Jiejie Xu, Jianxin Gu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 24 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

7 authors at 2 institutions in 1 country.

Weisi LiuDepartments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032.
Yidong LiuDepartments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032.
Haiou LiuShanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai 200011, China.
Weijuan ZhangDepartments of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032.
Qiang FuDepartments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032.
Jiejie XuDepartments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032. Electronic address: jjxufdu@fudan.edu.cn.
Jianxin GuDepartments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032.
Fudan University · CNObstetrics and Gynecology Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous studies identified the oncogenic role of p21-activated kinase 1 (PAK1) in hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC). Contrarily, PAK6 was found to predict a favorable prognosis in RCC patients. Nevertheless, the ambiguous tumor suppressive function of PAK6 in hepatocarcinogenesis remains obscure. Herein, decreased PAK6 expression was found to be associated with tumor node metastasis stage progression and unfavorable overall survival in HCC patients. Additionally, overexpression and silence of PAK6 experiments showed that PAK6 inhibited xenografted tumor growth in vivo, and restricted cell proliferation, colony formation, migration, and invasion and promoted cell apoptosis and anoikis in vitro. Moreover, overexpression of kinase dead and nuclear localization signal deletion mutants of PAK6 experiments indicated the tumor suppressive function of PAK6 was partially dependent on its kinase activity and nuclear translocation. Furthermore, gain or loss of function in polycomb repressive complex 2 (PRC2) components, including EZH2, SUZ12, and EED, elucidated epigenetic control of H3K27me3-arbitrated PAK6 down-regulation in hepatoma cells. More importantly, negative correlation between PAK6 and EZH2 expression was observed in hepatoma tissues from HCC patients. These data identified the tumor suppressive role and potential underlying mechanism of PAK6 in hepatocarcinogenesis.

Indexed as

Genes, Tumor SuppressorAnimalsCarcinoma, HepatocellularCell DivisionCell Line, TumorFemaleHeterograftsHumansLiver NeoplasmsMaleMiceMice, NudeMiddle Agedp21-Activated KinasesSurvival Ratep21-Activated KinasesPAK6 protein, humancancer biologyenhancer of zeste homolog 2hepatocellular carcinomahistone methylationoverall survivalpolycombprognostic factorserine/threonine-protein kinase PAK 6 (PAK6)

Identifiers

PMID26442588
PMCPMC4653705
OpenAlexW2179122166

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.