Evidence map›Paper›PMID 30545369›Full record

ArticleCell communication and signaling : CCS2018

Blockade of ARHGAP11A reverses malignant progress via inactivating Rac1B in hepatocellular carcinoma.

Bin Dai, Xuan Zhang, Runze Shang, Jianlin Wang, Xisheng Yang, Hong Zhang, Qi Liu, Desheng Wang, Lin Wang, Kefeng Dou

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

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  13. Protooncogenic Role ofBioMed research international · 2023
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  14. RHO GTPase family in hepatocellular carcinoma.Experimental hematology & oncology · 2022
    Review
  15. Article
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  18. Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022
    Review
  19. Article
  20. Article
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 2 institutions in 1 country.

Bin DaiDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Xuan ZhangDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Runze ShangDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Jianlin WangDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Xisheng YangDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Hong ZhangDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Qi LiuDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Desheng WangDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China. wangdesh@163.com.
Lin WangDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China. Fierywang@163.com.
Kefeng DouDepartment of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China. doukef@fmmu.edu.cn.
Xijing Hospital · CNAir Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe molecular signaling events involving in high malignancy and poor prognosis of hepatocellular carcinoma (HCC) are extremely complicated. Blockade of currently known targets has not yet led to successful clinical outcome. More understanding about the regulatory mechanisms in HCC is necessary for developing new effective therapeutic strategies for HCC patients.

methodsThe expression of Rho GTPase-activating protein 11A (ARHGAP11A) was examined in human normal liver and HCC tissues. The correlations between ARHGAP11A expression and clinicopathological stage or prognosis in HCC patients were analyzed. ARHGAP11A was downregulated to determine its role in the proliferation, invasion, migration, epithelial-to-mesenchymal transition (EMT) development, and regulatory signaling of HCC cells in vitro and in vivo.

resultsARHGAP11A exhibited high expression in HCC, and was significantly correlated with clinicopathological stage and prognosis in HCC patients. Moreover, ARHGAP11A facilitated Hep3B and MHCC97-H cell proliferation, invasion, migration and EMT development in vitro. ARHGAP11A knockdown significantly inhibited the in vivo growth and metastasis of HCC cells. Furthermore, ARHGAP11A directly interacted with Rac1B independent of Rho GTPase- activating activity. Rac1B blockade effectively interrupted ARHGAP11A-elicited HCC malignant phenotype. Meanwhile, upregulation of Rac1B reversed ARHGAP11A knockdown mediated mesenchymal-to-epithelial transition (MET) development in HCC cells.

conclusionARHGAP11A facilitates malignant progression in HCC patients via ARHGAP11A-Rac1B interaction. The ARHGAP11A/Rac1B signaling could be a potential therapeutic target in the clinical treatment of HCC.

Indexed as

Gene Knockdown TechniquesCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGTPase-Activating ProteinsHumansLiver NeoplasmsMaleMiddle AgedNeoplasm InvasivenessARHGAP11A protein, humanGTPase-Activating Proteinsrac1 GTP-Binding ProteinRAC1 protein, humanARHGAP11AEMTHepatocellular carcinomaMetastasisRac1B

Identifiers

PMID30545369
PMCPMC6293628
OpenAlexW2904546433

What OpenQuestion holds

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LicenceCC BY
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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.