Evidence map›Paper›PMID 26135947›Full record

ArticleGynecologic oncology2015

Glucose promotes cell proliferation, glucose uptake and invasion in endometrial cancer cells via AMPK/mTOR/S6 and MAPK signaling.

Jianjun Han, Lu Zhang, Hui Guo, Weiya Z Wysham, Dario R Roque, Adam K Willson, Xiugui Sheng, Chunxiao Zhou, Victoria L Bae-Jump

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gynecologic oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

124 citing papers in PubMed, 181 citations in OpenAlex.

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  12. Diabetes, Obesity, and Endometrial Cancer: A Review.Current oncology (Toronto, Ont.) · 2025
    Review
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64 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

9 authors at 2 institutions in 2 countries.

Jianjun HanDepartment of Surgical Oncology, Shandong Cancer Hospital and Institute, Jinan, China; Division of Gynecologic Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Lu ZhangDivision of Gynecologic Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; School of Medicine and Life Sciences, University of Jinan, Shandong Academy of Medical Sciences, China; Department of Gynecologic Oncology, Shandong Cancer Hospital and Institute, Jinan, China.
Hui GuoDivision of Gynecologic Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; School of Medicine and Life Sciences, University of Jinan, Shandong Academy of Medical Sciences, China; Department of Gynecologic Oncology, Shandong Cancer Hospital and Institute, Jinan, China.
Weiya Z WyshamDivision of Gynecologic Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Dario R RoqueDivision of Gynecologic Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Adam K WillsonDivision of Gynecologic Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Xiugui ShengDepartment of Gynecologic Oncology, Shandong Cancer Hospital and Institute, Jinan, China.
Chunxiao ZhouDivision of Gynecologic Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Electronic address: czhou@med.unc.edu.
Victoria L Bae-JumpDivision of Gynecologic Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Electronic address: victoria_baejump@med.unc.edu.
University of North Carolina at Chapel Hill · USShandong Tumor Hospital · CN

Funding

Metformin as a Novel Chemotheraeutic Strategy for the Treatment of Endometrial CaK23CA143154 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BAE-JUMP, VICTORIA LIN · 2010 to 2014
$854k
NCI NIH HHS 1K23CA143154-01A1NCI NIH HHS K23 CA143154
6 · The paper itself

Abstract

objectivesObesity and diabetes are well-known risk factors for the development of endometrial cancer. A high rate of aerobic glycolysis represents a key mechanism by which endometrial cancer cells consume glucose as its primary energy source. The up-regulated glycolytic pathway is a common therapeutic target whose inhibition has implications for anti-tumor activity in cancer cells. This study aimed to investigate the effect of various concentrations of glucose on cell proliferation in endometrial cancer.

methodsECC-1 and Ishikawa cells were treated with low glucose (1mM), normal glucose (5mM) and high glucose (25mM), and cytotoxicity, apoptosis, cell cycle, adhesion/invasion, and changes of AMPK/mTOR/S6 and MAPK pathways were evaluated.

resultsOur results revealed that high glucose increased cell growth and clonogenicity in two endometrial cancer cell lines in a dose dependent manner. Low glucose induced the activity of cleaved caspase 3 and caused cell cycle G1 arrest. High glucose increased the ability of adhesion and invasion by decreasing E-cadherin and increasing Snail expression. In addition, high glucose increased glucose uptake and glycolytic activity through modulating the AMPK/mTOR/S6 and MAPK pathways.

conclusionsOur findings suggest that glucose stimulated cell proliferation through multiple complex signaling pathways. Targeting glucose metabolism may be a promising therapeutic strategy in the treatment of endometrial cancer.

Indexed as

MAP Kinase Signaling SystemAMP-Activated Protein KinasesCell CycleCell Line, TumorCell ProliferationEndometrial NeoplasmsFemaleGlucoseGlycolysisHumansNeoplasm InvasivenessRibosomal Protein S6 KinasesRisk FactorsTOR Serine-Threonine KinasesAMP-Activated Protein KinasesGlucoseMTOR protein, humanRibosomal Protein S6 KinasesTOR Serine-Threonine KinasesEndometrial cancerGlucoseGlycolysisInvasion

Identifiers

PMID26135947
PMCPMC4672629
OpenAlexW1717177505

What OpenQuestion holds

Textmetadata
LicenceTDM
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.