Evidence map›Paper›PMID 28230863›Full record

ArticleCell death & disease2017

Oncogenic role of rab escort protein 1 through EGFR and STAT3 pathway.

Un-Jung Yun, Jee Young Sung, Seog-Yun Park, Sang-Kyu Ye, Jaegal Shim, Jae-Seon Lee, Masahiko Hibi, Young-Ki Bae, Yong-Nyun Kim

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Role of Rab GTPases in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2021
    Review
  6. Article
  7. Article
  8. 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 4 institutions in 2 countries.

Un-Jung YunComparative Biomedicine Research Branch, Division of Cancer Biology, National Cancer Center, Goyang, Korea.
Jee Young SungPediatric Oncology Branch, National Cancer Center, Goyang, Korea.
Seog-Yun ParkDepartment of Pathology, National Cancer Center, Goyang, Korea.
Sang-Kyu YeDepartment of Pharmacology, College of Medicine, Seoul National University, Seoul, Korea.
Jaegal ShimComparative Biomedicine Research Branch, Division of Cancer Biology, National Cancer Center, Goyang, Korea.
Jae-Seon LeeDepartment of Molecular Medicine, College of Medicine, Inha University, Incheon, Korea.
Masahiko HibiBioscience and Biotechnology Center, Nagoya University, Nagoya, Japan.
Young-Ki BaeComparative Biomedicine Research Branch, Division of Cancer Biology, National Cancer Center, Goyang, Korea.ORCID 0000-0001-7964-3540
Yong-Nyun KimComparative Biomedicine Research Branch, Division of Cancer Biology, National Cancer Center, Goyang, Korea.
National Cancer Center · KRInha University · KRNagoya University · JPSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rab escort protein-1 (REP1) is linked to choroideremia (CHM), an X-linked degenerative disorder caused by mutations of the gene encoding REP1 (CHM). REP1 mutant zebrafish showed excessive cell death throughout the body, including the eyes, indicating that REP1 is critical for cell survival, a hallmark of cancer. In the present study, we found that REP1 is overexpressed in human tumor tissues from cervical, lung, and colorectal cancer patients, whereas it is expressed at relatively low levels in the normal tissue counterparts. REP1 expression was also elevated in A549 lung cancer cells and HT-29 colon cancer cells compared with BEAS-2B normal lung and CCD-18Co normal colon epithelial cells, respectively. Interestingly, short interfering RNA (siRNA)-mediated REP1 knockdown-induced growth inhibition of cancer cell lines via downregulation of EGFR and inactivation of STAT3, but had a negligible effect on normal cell lines. Moreover, overexpression of REP1 in BEAS-2B cells enhanced cell growth and anchorage-independent colony formation with little increase in EGFR level and STAT3 activation. Furthermore, REP1 knockdown effectively reduced tumor growth in a mouse xenograft model via EGFR downregulation and STAT3 inactivation in vivo. These data suggest that REP1 plays an oncogenic role, driving tumorigenicity via EGFR and STAT3 signaling, and is a potential therapeutic target to control cancers.

Indexed as

A549 CellsAdaptor Proteins, Signal TransducingAnimalsCarcinogenesisCell LineCell Line, TumorCell ProliferationChoroideremiaDown-RegulationErbB ReceptorsHT29 CellsHumansMiceMice, Inbred BALB CMice, NudeMutationAdaptor Proteins, Signal TransducingCHM protein, humanEGFR protein, humanErbB ReceptorsSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID28230863
PMCPMC5386492
OpenAlexW2591548573

What OpenQuestion holds

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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.