Evidence map›Paper›PMID 26472188›Full record

ArticleOncotarget2015

Targeting EMP3 suppresses proliferation and invasion of hepatocellular carcinoma cells through inactivation of PI3K/Akt pathway.

Yi-Hsien Hsieh, Shu-Ching Hsieh, Chien-Hsing Lee, Shun-Fa Yang, Chun-Wen Cheng, Meng-Ju Tang, Chia-Liang Lin, Chu-Liang Lin, Ruey-Hwang Chou

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

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  5. EMP3: A promising biomarker for tumor prognosis and targeted cancer therapy.Cancer biomarkers : section A of Disease markers · 2024
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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

9 authors at 4 institutions in 1 country.

Yi-Hsien HsiehDepartment of Biochemistry, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Shu-Ching HsiehInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Chien-Hsing LeeGraduate Institute of Medical Sciences, Chang Jung Christian University, Tainan, Taiwan.
Shun-Fa YangInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Chun-Wen ChengInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Meng-Ju TangInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chia-Liang LinInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chu-Liang LinInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Ruey-Hwang ChouGraduate Institute of Cancer Biology and Center for Molecular Medicine, China Medical University, Taichung, Taiwan.
Chung Shan Medical University · TWAsia University · TWChina Medical University · TWChung Shan Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial membrane protein-3 (EMP3), a typical member of the epithelial membrane protein (EMP) family, is epigenetically silenced in some cancer types, and has been proposed to be a tumor suppressor gene. However, its effects on tumor suppression are controversial and its roles in development and malignancy of hepatocellular carcinoma (HCC) remain unclear. In the present study, we found that EMP3 was highly expressed in the tumorous tissues comparing to the matched normal tissues, and negatively correlated with differentiated degree of HCC patients. Knockdown of EMP3 significantly reduced cell proliferation, arrested cell cycle at G1 phase, and inhibited the motility and invasiveness in accordance with the decreased expression and activity of urokinase plasminogen activator (uPA) and matrix metalloproteinase 9 (MMP-9) in HCC cells. The in vivo tumor growth of HCC was effectively suppressed by knockdown of EMP3 in a xenograft mouse model. The EMP3 knockdown-reduced cell proliferation and invasion were attenuated by inhibition of phosphatidylinositol 3-kinase (PI3K) or knockdown of Akt, and rescued by overexpression of Akt in HCC cells. Clinical positive correlations of EMP3 with p85 regulatory subunit of PI3K, p-Akt, uPA, as well as MMP-9 were observed in the tissue sections from HCC patients. Here, we elucidated the tumor progressive effects of EMP3 through PI3K/Akt pathway and uPA/MMP-9 cascade in HCC cells. The findings provided a new insight into EMP3, which might be a potential molecular target for diagnosis and treatment of HCC.

Indexed as

AgedAnimalsBlotting, WesternCarcinoma, HepatocellularCell ProliferationFemaleFlow CytometryFluorescent Antibody TechniqueGene Knockdown TechniquesHeterograftsHumansImmunoprecipitationLiver NeoplasmsMaleMembrane GlycoproteinsMiceEMP3 protein, humanMembrane GlycoproteinsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktepithelial membrane protein-3hepatocellular carcinomainvasionmigrationproliferation

Identifiers

PMID26472188
PMCPMC4741495
OpenAlexW2265596009

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.