Evidence map›Paper›PMID 27602956›Full record

ArticleOncotarget2016

Urokinase-type plasminogen activator receptor promotes proliferation and invasion with reduced cisplatin sensitivity in malignant mesothelioma.

Shenqi Wang, Li Jiang, Yipeng Han, Shan Hwu Chew, Yuuki Ohara, Shinya Akatsuka, Liang Weng, Koji Kawaguchi, Takayuki Fukui, Yoshitaka Sekido and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Shenqi WangDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Li JiangDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Yipeng HanDepartment of Tumor Pathology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Shan Hwu ChewDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Yuuki OharaDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Shinya AkatsukaDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Liang WengDepartment of Tumor Pathology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Koji KawaguchiDepartment of Thoracic Surgery, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Takayuki FukuiDepartment of Thoracic Surgery, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Yoshitaka SekidoDepartment of Cancer Genetics, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Kohei YokoiDepartment of Thoracic Surgery, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Shinya ToyokuniDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant mesothelioma (MM) is a rare neoplasm associated with asbestos exposure. The prognosis of MM is poor because it is aggressive and highly resistant to chemotherapy. Using a rat model of asbestos-induced MM, we found elevated urokinase-type plasminogen activator receptor (uPAR; Plaur) expression in rat tissues, which was associated with poor prognosis. The proliferation, migration and invasion of MM cells were suppressed by uPAR knockdown and increased by overexpression experiments, irrespective of urokinase-type plasminogen activator (uPA; Plau) levels. More importantly, we found that uPAR expression is associated with sensitivity to cisplatin in MM through the PI3K/AKT pathway, which was demonstrated with specific inhibitors, LY294002 and Akti-1/2. uPAR knockdown significantly increased sensitivity to cisplatin whereas its overexpression significantly decreased cisplatin sensitivity. Furthermore, sera and tissues from MM patients showed significantly high uPAR levels, which suggested the pathogenic role of uPAR in the tumor biology of human MM. In conclusion, our findings indicate that uPAR levels are associated with malignant characteristics and cisplatin sensitivity of MM. In addition to the potential use of uPAR as a prognostic marker, the combination of uPAR abrogation and cisplatin may reveal a promising therapeutic approach for MM.

Indexed as

AnimalsAntineoplastic AgentsApoptosisAsbestosCell Line, TumorCell ProliferationCisplatinGene Expression ProfilingGene Expression Regulation, NeoplasticHumansLung NeoplasmsMesotheliomaMesothelioma, MalignantMice, Inbred BALB CMice, NudeNeoplasm InvasivenessAntineoplastic AgentsAsbestosCisplatinReceptors, Urokinase Plasminogen ActivatorAKT signaling pathwaycisplatinmalignant mesotheliomauPAR

Identifiers

PMID27602956
PMCPMC5342498
OpenAlexW2516792275

What OpenQuestion holds

Textmetadata
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.