Evidence map›Paper›PMID 31841274›Full record

ArticleThoracic cancer2020

Downregulation of Rab17 promotes cell proliferation and invasion in non-small cell lung cancer through STAT3/HIF-1α/VEGF signaling.

Mingliang Wang, Wendong Wang, Jingmin Ding, Jiashun Wang, Jun Zhang

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-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

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Erbin Inhibited AngiogenesisCurrent medicinal chemistry · 2026
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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

5 authors at 1 institution in 1 country.

Mingliang WangDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Wendong WangDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jingmin DingDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jiashun WangDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jun ZhangDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0001-7915-9476
Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRab GTPases play a key role in regulating intercellular vesicle trafficking in both exo- and endocytic pathways. Recent studies have reported that Rab small GTPases and the associated regulatory proteins and effectors are involved in many cancers. The purpose of this study was to investigate the biological role of Rab17 in non-small cell lung cancer (NSCLC) and the relative mechanism.

methodsRab17 expression in human NSCLC cell lines and tissues was evaluated using real-time PCR (RT-PCR), western blot and immunohistochemical (IHC) staining. NSCLC cell lines with RAB17 stable knockdown were generated to explore its function in vitro and in vivo. Additionally, we investigated the potential mechanism of Rab17 by identifying the expression levels of STAT3/HIF-1α/VEGF pathway using western blot analysis.

resultsDecreased Rab17 expression was correlated with poor overall survival in NSCLC patients. The functional assays showed that knockdown of Rab17 could promote tumorigenic properties of NSCLC cells in vitro and in vivo, including enhanced cell proliferation, colony formation, invasion and migration, angiogenesis and tumor xenograft growth, and suppressed apoptosis. Moreover, Rab17 downregulation decreased epithelial marker E-cadherin and increased mesenchymal markers Vimentin and β-catenin, suggesting knockdown of Rab17 induced epithelial-mesenchymal transition (EMT).

conclusionDownregulation of Rab17 promotes cell invasion and enhances tumorigenicity in part through the STAT3/HIF-1α/VEGF pathway, which may represent a novel potential therapeutic target.

Indexed as

AnimalsApoptosisBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitLung NeoplasmsMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessPrognosisBiomarkers, TumorHIF1A protein, humanHypoxia-Inducible Factor 1, alpha Subunitrab17 protein, epithelialrab GTP-Binding ProteinsSTAT3 protein, humanSTAT3 Transcription FactorVascular Endothelial Growth Factor AVEGFA protein, humanangiogenesisinvasionNSCLCRab17STAT3/HIF-1α/VEGF

Identifiers

PMID31841274
PMCPMC6997001
OpenAlexW2995947279

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.