Evidence map›Paper›PMID 25841765›Full record

ArticleMolecular oncology2015

Plasma membrane gp96 enhances invasion and metastatic potential of liver cancer via regulation of uPAR.

Junwei Hou, Xin Li, Changfei Li, Lu Sun, Yulai Zhao, Jingmin Zhao, Songdong Meng

Open access · bronzeAbstract read
In one paragraph

Article in Molecular oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-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

19 citing papers in PubMed, 29 citations in OpenAlex.

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  17. Clients and Oncogenic Roles of Molecular Chaperone gp96/grp94.Current topics in medicinal chemistry · 2016
    Review
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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

7 authors at 2 institutions in 1 country.

Junwei HouCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, PR China.
Xin LiCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, PR China.
Changfei LiCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, PR China.
Lu SunCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, PR China.
Yulai ZhaoInstitute of Infectious Diseases, Beijing 302 Hospital, Beijing, PR China.
Jingmin ZhaoInstitute of Infectious Diseases, Beijing 302 Hospital, Beijing, PR China. Electronic address: jmzhao302@163.com.
Songdong MengCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, PR China. Electronic address: mengsd@im.ac.cn.
Chinese Academy of Sciences · CN302 Military Hospital of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeted therapy is currently under intensive investigation due to the resistance of liver cancer to cytotoxic chemotherapies. Dissecting the molecular events that drive the progression of liver cancer and defining specific targets are urgently needed to develop efficient tailored therapies. Cell membrane gp96 (mgp96) has been implicated in tumor growth and malignancy. Here, we explored the functional and clinical relevance of mgp96 in liver cancer. We found that elevated mgp96 abundance was associated with tumor metastasis and recurrence in patients with primary liver tumors. Decreased KDELR1 levels in hepatoma cells contribute to cell membrane translocation of the normally ER-resident gp96. Urokinase-type plasminogen activator receptor (uPAR) was identified as a mgp96 client protein, and mgp96 stabilized uPAR protein. Our clinical results proved that elevated mgp96 abundance is positively correlated with uPAR expression levels in liver tumors. We further provided evidence that targeting mgp96 with siRNA or a specific mAb that blocked the mgp96-uPAR interaction led to inhibited cell growth, survival, and invasion in vitro, as well as the suppression of liver tumor growth and metastasis in vivo. mgp96 promotes liver cancer progression through increasing the protein stability and signaling of uPAR, and may be a new promising target for suppressing uPAR-mediated tumor growth and metastasis in liver cancer.

Indexed as

AnimalsCell Line, TumorCell ProliferationFemaleGene Knockdown TechniquesHumansLiver NeoplasmsMaleMembrane GlycoproteinsMice, Inbred BALB CMiddle AgedNeoplasm InvasivenessNeoplasm MetastasisReceptors, Urokinase Plasminogen ActivatorendoplasminMembrane GlycoproteinsReceptors, Urokinase Plasminogen ActivatorDFSLiver cancerMAPKmgp96uPAR

Identifiers

PMID25841765
PMCPMC5528822
OpenAlexW2161835398

What OpenQuestion holds

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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.