Evidence map›Paper›PMID 30206221›Full record

ArticleCell death & disease2018

ARHGAP9 suppresses the migration and invasion of hepatocellular carcinoma cells through up-regulating FOXJ2/E-cadherin.

Hong Zhang, Qing-Feng Tang, Meng-Yao Sun, Chun-Yan Zhang, Jian-Yong Zhu, Yu-Li Shen, Bin Zhao, Zhi-Yi Shao, Li-Jun Zhang, Hong Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

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  11. Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022
    Review
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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 1 institution in 1 country.

Hong ZhangCentral Laboratory, Seventh People's Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200137, China.
Qing-Feng TangDepartment of Clinical Laboratory and Central Laboratory, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, China.
Meng-Yao SunDepartment of Clinical Laboratory and Central Laboratory, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, China.
Chun-Yan ZhangCentral Laboratory, Seventh People's Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200137, China.
Jian-Yong ZhuCentral Laboratory, Seventh People's Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200137, China.
Yu-Li ShenCentral Laboratory, Seventh People's Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200137, China.
Bin ZhaoDepartment of General Surgery, Seventh People's Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200137, China.
Zhi-Yi ShaoCentral Laboratory, Seventh People's Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200137, China.
Li-Jun ZhangCentral Laboratory, Seventh People's Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200137, China. zhanglijun0407@163.com.
Hong ZhangCentral Laboratory, Seventh People's Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200137, China. lkzhang97@126.com.
Shanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rho GTPase activating protein 9 (ARHGAP9), a member of RhoGAP family, has been identified as a RhoGAP for Cdc42 and Rac1. Here, we aimed to clarify the expression and functional role of ARHGAP9 in hepatocellular carcinoma (HCC). By analyzing TCGA (The Cancer Genome Atlas) LIHC (liver hepatocellular carcinoma) database, we found that ARHGAP9 expression was lower in HCC tissues than in normal liver tissues, and that patients with ARHGAP9 lower expression had a significant shorter overall survival time than those with ARHGAP9 higher expression. Cell counting kit-8 (CCK-8), transwell assays and in vivo experimental lung metastasis assay revealed that ARHGAP9 overexpression could inhibit HCC cell proliferation, migration and invasion, as well as HCC lung metastases. By next-generation RNA-sequencing, we identified that a transcription factor, Forkhead Box J2 (FOXJ2), was significantly induced by ARHGAP9 overexpression in HepG2 cells. Ectopic expression of FOXJ2 in HCC cell lines also exerted inhibitory effects on cell migration and invasion. Moreover, the inhibitory effects of ARHGAP9 on HCC cell migration and invasion was significantly attenuated by FOXJ2 knockdown. Luciferase reporter assay demonstrated that ARHGAP9 enhanced the transcription of E-cadherin (CDH1) via FOXJ2. Chromatin immunoprecipitation (ChIP) assay demonstrated that FOXJ2 modulated the transcription of E-cadherin (CDH1) by directly binding to its promoter. Furthermore, Pearson's correlation analysis indicated that the mRNA levels of ARHGAP9 in HCC tissues were positively correlated with the mRNA levels of FOXJ2 and CDH1. These data clearly show that ARHGAP9/FOXJ2 inhibit cell migration and invasion during HCC development via inducing the transcription of CDH1.

Indexed as

AnimalsAntigens, CDCadherinsCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationForkhead Transcription FactorsGene Expression Regulation, NeoplasticGTPase-Activating ProteinsHep G2 CellsHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CAntigens, CDARHGAP9 protein, humanCadherinsCDH1 protein, humanForkhead Transcription FactorsFOXJ2 protein, humanGTPase-Activating Proteins

Identifiers

PMID30206221
PMCPMC6133947
OpenAlexW2889935537

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.