Evidence map›Paper›PMID 25394504›Full record

ArticleCancer gene therapy2014

Knockdown of EGFR inhibits growth and invasion of gastric cancer cells.

Y Zhen, L Guanghui, Z Xiefu

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

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  13. The combinational therapy of trastuzumab and cetuximab inhibits tumor growth in a patient-derived tumor xenograft model of gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016
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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

3 authors at 1 institution in 1 country.

Y ZhenDepartment of Gastroenterological Surgery, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
L GuanghuiDepartment of Gastroenterological Surgery, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Z XiefuDepartment of Gastroenterological Surgery, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) is an oncogenic trans-membranous receptor, which is overexpressed in multiple human cancers. However, the role of EGFR in gastric cancer (GC) is still elusive. In this study, we aimed to investigate the expression and molecular mechanisms of EGFR in GC cells. Forty cases of GC and the corresponding adjacent non-cancerous tissues (ANCT) were collected, and the expression of EGFR was assessed using immunohistochemistry in biopsy samples. Furthermore, EGFR signaling was blocked by constructed recombinant small hairpin RNA lentiviral vector (Lv-shRAGE) used to transfect into human GC SGC-7901 cells. The expression of AKT, proliferating cell nuclear antigen (PCNA) and matrix metallopeptidase-9 (MMP-9) was detected by real-time PCR and western blotting assays. Cell proliferative activities and invasive capability were, respectively, determined by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) and Transwell assays. Cell apoptosis and cycle distribution were analyzed by flow cytometry. EGFR was found highly expressed in cancer tissues compared with the ANCT and correlated with lymph node metastases. Knockdown of EGFR reduced cell proliferation and invasion of GC with decreased expression of AKT, PCNA and MMP-9 and induced cell apoptosis and cycle arrest. Upregulation of EGFR expression is associated with lymph node metastases of GC, and blockade of EGFR signaling suppresses growth and invasion of GC cells through AKT pathway, suggesting that EGFR may represent a potential therapeutic target for this aggressive malignancy.

Indexed as

Blotting, WesternCell ProliferationErbB ReceptorsGene Expression Regulation, NeoplasticGene Knockdown TechniquesGenetic VectorsHumansImmunohistochemistryLentivirusMatrix Metalloproteinase 9Neoplasm InvasivenessProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-aktReal-Time Polymerase Chain ReactionRNA, Small InterferingSignal TransductionErbB ReceptorsMatrix Metalloproteinase 9Proliferating Cell Nuclear AntigenProto-Oncogene Proteins c-aktRNA, Small InterferingTetrazolium SaltsThiazolesthiazolyl blue

Identifiers

PMID25394504
OpenAlexW1976913341

What OpenQuestion holds

Textmetadata
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.