Evidence map›Paper›PMID 26443539›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Overexpression of Rab5a promotes hepatocellular carcinoma cell proliferation and invasion via FAK signaling pathway.

Donghua Geng, Wenyan Zhao, Yong Feng, Jingang Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. 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
1.1field-weighted citation impact, top 25% 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, 19 citations in OpenAlex.

  1. Review
  2. Article
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  7. Review
  8. Review
  9. Article
  10. Expression of Rab5a correlates with tumor progression in pancreatic carcinoma.Virchows Archiv : an international journal of pathology · 2017
    Article
  11. Review
  12. Review
  13. Rap2B promotes cell proliferation, migration and invasion in prostate cancer.Medical oncology (Northwood, London, England) · 2016
    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

4 authors at 1 institution in 1 country.

Donghua GengDepartment of Surgery, The Affiliated Shengjing Hospital of China Medical University, Sanhao Street 36, Shenyang, 110004, Liaoning Province, PR China.
Wenyan ZhaoDepartment of Surgery, The Affiliated Shengjing Hospital of China Medical University, Sanhao Street 36, Shenyang, 110004, Liaoning Province, PR China.
Yong FengDepartment of Surgery, The Affiliated Shengjing Hospital of China Medical University, Sanhao Street 36, Shenyang, 110004, Liaoning Province, PR China. fengyong_sj@163.com.
Jingang LiuDepartment of Surgery, The Affiliated Shengjing Hospital of China Medical University, Sanhao Street 36, Shenyang, 110004, Liaoning Province, PR China. liujgcmu@yeah.net.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rab5a was reported to be overexpressed in human malignancy and associated with the malignant phenotype. To data, its expression pattern and biological function in hepatocellular carcinoma (HCC) have not been studied. We analyzed Rab5a protein expression in 98 cases of HCC tissues and four HCC cell lines. We found that Rab5a expression was upregulated in HCC tissues and cell lines. Rab5a overexpression correlated with TNM stage and nodal metastasis (p < 0.05). To confirm the biological function of Rab5a in HCC cell lines, Rab5a siRNA was employed in SK-Hep-1 cell line and plasmid transfection was performed in Huh7 cell line. CCK-8 assay showed that Rab5a depletion blocked cell growth rate while Rab5a overexpression facilitated proliferation. Transwell and migration assay showed that Rab5a positively regulated cell invasion and migration. To explore the molecular mechanism underlying the biological effects of Rab5a, we checked several signaling pathways and found that Rab5a overexpression upregulated cyclin D1, cyclin E expression, FAK (Tyr397), and AKT (Ser473) phosphorylation. Blockage of FAK using inhibitor PF573228 abolished the role of Rab5a on cyclin D1. In conclusion, Rab5a is overexpressed in human HCC and contributes to cancer cell proliferation and invasion through regulation of FAK and AKT signaling.

Indexed as

Blotting, WesternCarcinoma, HepatocellularCell LineCell Line, TumorCell MovementCell ProliferationCyclin D1Focal Adhesion Kinase 1Gene Expression Regulation, NeoplasticHep G2 CellsHumansImmunohistochemistryLiver NeoplasmsNeoplasm InvasivenessProto-Oncogene Proteins c-aktrab5 GTP-Binding ProteinsCyclin D1Focal Adhesion Kinase 1Proto-Oncogene Proteins c-aktPTK2 protein, humanRAB5C protein, humanrab5 GTP-Binding ProteinsFAKHepatocellular carcinomaRab5a

Identifiers

PMID26443539
OpenAlexW1871181733

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.