Evidence map›Paper›PMID 25887760›Full record

ArticleJournal of hematology & oncology2015

Alpha-enolase promotes cell glycolysis, growth, migration, and invasion in non-small cell lung cancer through FAK-mediated PI3K/AKT pathway.

Qiao-Fen Fu, Yan Liu, Yue Fan, Sheng-Ni Hua, Hong-Ying Qu, Su-Wei Dong, Rui-Lei Li, Meng-Yang Zhao, Yan Zhen, Xiao-Li Yu and 8 more

Open access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

164 citing papers in PubMed, 300 citations in OpenAlex.

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  10. SENP1 drives glycolysis and cisplatin resistance in gastric cancer via desumoylating ENO1.Journal of experimental & clinical cancer research : CR · 2025
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104 more citing papers are in PubMed but not listed here.

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

18 authors at 4 institutions in 1 country.

Qiao-Fen FuCancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Guangdong, People's Republic China. fuqiaofen@163.com.
Yan LiuCancer Research Institute of Southern Medical University, Guangzhou, Guangdong, People's Republic China. echo0516@sina.com.
Yue FanCancer Research Institute of Southern Medical University, Guangzhou, Guangdong, People's Republic China. 258173709@qq.com.
Sheng-Ni HuaCancer Research Institute of Southern Medical University, Guangzhou, Guangdong, People's Republic China. 690253346@qq.com.
Hong-Ying QuCancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Guangdong, People's Republic China. Quhongying2005@sina.com.
Su-Wei DongCancer Research Institute of Southern Medical University, Guangzhou, Guangdong, People's Republic China. 290019049@qq.com.
Rui-Lei LiDepartment of Cancer Biotherapy Center, Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan, People's Republic China. 317178823@qq.com.
Meng-Yang ZhaoCancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Guangdong, People's Republic China. 879299359@qq.com.
Yan ZhenCancer Research Institute of Southern Medical University, Guangzhou, Guangdong, People's Republic China. 915226808@qq.com.
Xiao-Li YuCancer Research Institute of Southern Medical University, Guangzhou, Guangdong, People's Republic China. 158851881@qq.com.
Yi-Yu ChenCancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Guangdong, People's Republic China. 315108408@qq.com.
Rong-Cheng LuoCancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Guangdong, People's Republic China. beautiful198711@163.com.
Rong LiCancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Guangdong, People's Republic China. rongxin1003@163.com.
Li-Bo LiCancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Guangdong, People's Republic China. mifeihehe0808@126.com.
Xiao-Jie DengCancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Guangdong, People's Republic China. sophiexiaojie@qq.com.
Wei-Yi FangCancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Guangdong, People's Republic China. fangweiyi1975@163.com.
Zhen LiuCancer Research Institute of Southern Medical University, Guangzhou, Guangdong, People's Republic China. narcissus_jane@163.com.
Xin SongCancer Research Institute of Southern Medical University, Guangzhou, Guangdong, People's Republic China. songxin68@126.com.
Southern Medical University · CNTCM-Intigrated Cancer Center of Southern Medical University · CNGuangzhou Medical University · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDuring tumor formation and expansion, increasing glucose metabolism is necessary for unrestricted growth of tumor cells. Expression of key glycolytic enzyme alpha-enolase (ENO1) is controversial and its modulatory mechanisms are still unclear in non-small cell lung cancer (NSCLC).

methodsThe expression of ENO1 was examined in NSCLC and non-cancerous lung tissues, NSCLC cell lines, and immortalized human bronchial epithelial cell (HBE) by quantitative real-time reverse transcription PCR (qRT-PCR), immunohistochemistry, and Western blot, respectively. The effects and modulatory mechanisms of ENO1 on cell glycolysis, growth, migration, invasion, and in vivo tumorigenesis and metastasis in nude mice were also analyzed.

resultsENO1 expression was increased in NSCLC tissues in comparison to non-cancerous lung tissues. Similarly, NSCLC cell lines A549 and SPCA-1 also express higher ENO1 than HBE cell line in both mRNA and protein levels. Overexpressed ENO1 significantly elevated NSCLC cell glycolysis, proliferation, clone formation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo by regulating the expression of glycolysis, cell cycle, and epithelial-mesenchymal transition (EMT)-associated genes. Conversely, ENO1 knockdown reversed these effects. More importantly, our further study revealed that stably upregulated ENO1 activated FAK/PI3K/AKT and its downstream signals to regulate the glycolysis, cell cycle, and EMT-associated genes.

conclusionThis study showed that ENO1 is responsible for NSCLC proliferation and metastasis; thus, ENO1 might serve as a potential molecular therapeutic target for NSCLC treatment.

Indexed as

AnimalsBiomarkers, TumorBlotting, WesternCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationDNA-Binding ProteinsFocal Adhesion Kinase 1GlycolysisHeterograftsHumansImmunohistochemistryLung NeoplasmsMiceMice, NudeBiomarkers, TumorDNA-Binding ProteinsENO1 protein, humanFocal Adhesion Kinase 1Phosphatidylinositol 3-KinasesPhosphopyruvate HydrataseProto-Oncogene Proteins c-aktPTK2 protein, humanRNA, Small InterferingTumor Suppressor Proteins

Identifiers

PMID25887760
PMCPMC4359783
OpenAlexW2167219679

What OpenQuestion holds

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LicenceCC BY
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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.