Evidence map›Paper›PMID 26191189›Full record

ArticleInternational journal of clinical and experimental pathology2015

Down-regulation of Rab17 promotes tumourigenic properties of hepatocellular carcinoma cells via Erk pathway.

Jingsong Qi, Peng Zhao, Fenbao Li, Yingchang Guo, Hongkai Cui, Aiguang Liu, Huajie Mao, Yongli Zhao, Xizhong Zhang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

9 authors at 1 institution in 1 country.

Jingsong QiDepartment of Intervention, The First Hospital Affiliated to The Xinxiang Medical University Xinxiang, Henan, China.
Peng ZhaoDepartment of Intervention, The First Hospital Affiliated to The Xinxiang Medical University Xinxiang, Henan, China.
Fenbao LiDepartment of Intervention, The First Hospital Affiliated to The Xinxiang Medical University Xinxiang, Henan, China.
Yingchang GuoDepartment of Intervention, The First Hospital Affiliated to The Xinxiang Medical University Xinxiang, Henan, China.
Hongkai CuiDepartment of Intervention, The First Hospital Affiliated to The Xinxiang Medical University Xinxiang, Henan, China.
Aiguang LiuDepartment of Intervention, The First Hospital Affiliated to The Xinxiang Medical University Xinxiang, Henan, China.
Huajie MaoDepartment of Intervention, The First Hospital Affiliated to The Xinxiang Medical University Xinxiang, Henan, China.
Yongli ZhaoDepartment of Intervention, The First Hospital Affiliated to The Xinxiang Medical University Xinxiang, Henan, China.
Xizhong ZhangDepartment of Intervention, The First Hospital Affiliated to The Xinxiang Medical University Xinxiang, Henan, China.
First Affiliated Hospital of Xinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The small GTPase, Ras-related protein 17 (Rab17), a member of the Rab family, plays a critical role in the regulation of membrane traffic in polarized eukaryotic cells. However, the role of Rab17 in hepatocellular carcinoma (HCC) is not clear. Clinical speciments reveal that Rab17 was present in 15 of 20 (75.0%) paraneoplastic tissues and 7 of 20 (35.0%) HCC samples (P=0.0248). To elucidate the tumourigenic role of Rab17 in HCC, we generated two Rab17 low-expressing HCC cell lines (Hep3B and Huh-7). The results showed that Rab17 down-regulation significantly promoted the tumourigenic properties of HCC cells in vitro and in vivo, as demonstrated by enhanced cell proliferation, colony formation, invasion and migration, decreased G1 arrest, and increased tumour xenograft growth and angiogenesis. However, the enhanced tumourigenic properties of HCC cells by Rab17 down-regulation was significantly inhibited by PD980592, the inhibitor of the Erk pathway, indicating that the Erk pathway plays a critical role in Rab17 down-regulation-induced enhanced tumourigenic properties of HCC cells. Our data provide a new insight into the essential role of Rab17 in HCC carcinogenesis and suggest that Rab17 expression might be tumor suppressor gene and might provide a new interventional therapeutic target for this common malignancy.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationDown-RegulationExtracellular Signal-Regulated MAP KinasesG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMice, NudeNeoplasm InvasivenessAntineoplastic AgentsExtracellular Signal-Regulated MAP KinasesProtein Kinase Inhibitorsrab17 protein, epithelialrab GTP-Binding Proteinscell polarizationhepatocellular carcinoma cellsinterventional therapyRab17signaling pathwaysmall GTPase

Identifiers

PMID26191189
PMCPMC4503061
OpenAlexW2410826865

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.