Evidence map›Paper›PMID 28103577›Full record

ArticleOncotarget2017

Association of RAB5 overexpression in pancreatic cancer with cancer progression and poor prognosis via E-cadherin suppression.

Takamichi Igarashi, Kenichiro Araki, Takehiko Yokobori, Bolag Altan, Takahiro Yamanaka, Norihiro Ishii, Mariko Tsukagoshi, Akira Watanabe, Norio Kubo, Tadashi Handa and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

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  13. RAC1-GTP promotes epithelial-mesenchymal transition and invasion of colorectal cancer by activation of STAT3.Laboratory investigation; a journal of technical methods and pathology · 2018
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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

15 authors at 3 institutions in 1 country.

Takamichi IgarashiDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Kenichiro ArakiDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Takehiko YokoboriDivision of Integrated Oncology Research, Gunma University Initiative for Advanced Research, Maebashi, Gunma, Japan.
Bolag AltanIntegrative Center of General Surgery, Gunma University Hospital, Maebashi, Gunma, Japan.
Takahiro YamanakaDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Norihiro IshiiDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Mariko TsukagoshiDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Akira WatanabeDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Norio KuboDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Tadashi HandaDepartment of Diagnostic Pathology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Yasuo HosouchiDepartment of Surgery and Laparoscopic Surgery, Gunma Prefecture Saiseikai-Maebashi Hospital, Maebashi, Gunma, Japan.
Masahiko NishiyamaDepartment of Molecular Pharmacology and Oncology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Tetsunari OyamaDepartment of Diagnostic Pathology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Ken ShirabeDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Hiroyuki KuwanoIntegrative Center of General Surgery, Gunma University Hospital, Maebashi, Gunma, Japan.
Gunma University · JPGunma University Hospital · JPGunma Saiseikai Maebashi Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer is a common type of cancer with poor prognosis worldwide. Postoperative survival depends on the existence of metastasis. Elucidation of the mechanism underlying cancer progression is important to improve prognosis. The RAS-associated protein RAB5 activates intracellular membrane trafficking, and RAB5 expression is correlated to progression and epithelial mesenchymal transition in various cancers.The expression of RAB5 and E-cadherin in 111 pancreatic cancer samples was investigated by immunohistochemical staining, and the relationship among RAB5 expression, clinicopathological factors, and E-cadherin expression was assessed. Furthermore, RAB5 suppression analysis by siRNA was performed to determine the roles of RAB5 in morphological change, proliferation potency, cell migration ability, and invasiveness of the pancreatic cancer cell line.High RAB5 expression correlated with the presence of lymphatic invasion and venous invasion and low E-cadherin expression. Patients with high RAB5 expression had a poorer prognosis than those with low RAB5 expression. RAB5 suppression in pancreatic cancer cells enhanced E-cadherin expression; changed cell morphology from spindle to round; and inhibited proliferation, invasion, and cell migration.RAB5 contributes to poor prognosis and progression in pancreatic cancer patients. It may be a promising candidate for individualized therapy in refractory pancreatic cancer.

Indexed as

AdultAgedAged, 80 and overAntigens, CDBlotting, WesternCadherinsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansImmunohistochemistryMaleMicroscopy, FluorescenceAntigens, CDCadherinsCDH1 protein, humanRAB5C protein, humanrab5 GTP-Binding Proteinscancer progressionE-cadherinepithelial mesenchymal transitionpancreatic cancerRAB5

Identifiers

PMID28103577
PMCPMC5355344
OpenAlexW2577142196

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.