Evidence map›Paper›PMID 25593464›Full record

ArticleWorld journal of gastroenterology2015

E2F-1 overexpression inhibits human gastric cancer MGC-803 cell growth in vivo.

Wei-Yuan Wei, Lin-Hai Yan, Xiao-Tong Wang, Lei Li, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Yu-Bo Xie, Qiang Xiao

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2015. 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 20% 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, 15 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

10 authors at 1 institution in 1 country.

Wei-Yuan WeiWei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Lin-Hai YanWei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Xiao-Tong WangWei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Lei LiWei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Wen-Long CaoWei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Xiao-Shi ZhangWei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Ze-Xu ZhanWei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Han YuWei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Yu-Bo XieWei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Qiang XiaoWei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
World Wide Web Consortium · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo evaluate the influence of E2F-1 on the growth of human gastric cancer (GC) cells in vivo and the mechanism involved.

methodsE2F-1 recombinant lentiviral vectors were injected into xenograft tumors of MGC-803 cells in nude mice, and then tumor growth was investigated. Overexpression of transcription factor E2F-1 was assessed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting analysis. Apoptosis rates were determined using a terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay. Expression levels of certain cell cycle regulators and apoptosis-related proteins, such as Bax, survivin, Bcl-2, cyclin D1, S-phase kinase-associated protein 2, and c-Myc were examined by Western blotting and RT-PCR.

resultsXenograft tumors of MGC-803 cells in nude mice injected with E2F-1 recombinant lentiviral vectors stably overexpressed the E2F-1 gene as measured by semi-quantitative RT-PCR (relative mRNA expression: 0.10 ± 0.02 vs 0.05 ± 0.02 for control vector and 0.06 ± 0.03 for no infection; both P < 0.01) and Western blotting (relative protein expression: 1.90 ± 0.05 vs 1.10 ± 0.03 in control vector infected and 1.11 ± 0.02 for no infection; both P < 0.01). The growth-curve of tumor volumes revealed that infection with E2F-1 recombinant lentiviral vectors significantly inhibited the growth of human GC xenografts (2.81 ± 1.02 vs 6.18 ± 1.15 in control vector infected and 5.87 ± 1.23 with no infection; both P < 0.05) at 15 d after treatment. TUNEL analysis demonstrated that E2F-1 overexpression promoted tumor cell apoptosis (18.6% ± 2.3% vs 6.7% ± 1.2% in control vector infected 6.3% ± 1.2% for no infection; both P < 0.05). Furthermore, lentiviral vector-mediated E2F-1 overexpression increased the expression of Bax and suppressed survivin, Bcl-2, cyclin D1, Skp2, and c-Myc expression in tumor tissue.

conclusionE2F-1 inhibits growth of GC cells via regulating multiple signaling pathways, and may play an important role in targeted therapy for GC.

Indexed as

Cell ProliferationAnimalsApoptosisApoptosis Regulatory ProteinsCell CycleCell Cycle ProteinsCell Line, TumorE2F1 Transcription FactorGene Expression Regulation, NeoplasticHumansMice, Inbred BALB CMice, NudeRNA, MessengerSignal TransductionStomach NeoplasmsTime FactorsApoptosis Regulatory ProteinsCell Cycle ProteinsE2F1 protein, humanE2F1 Transcription FactorRNA, MessengerE2F-1Gastric cancerLentiviral vectorMouse model

Identifiers

PMID25593464
PMCPMC4292280
OpenAlexW2066890717

What OpenQuestion holds

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Registered trials

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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.