Evidence map›Paper›PMID 32581586›Full record

ArticleCancer management and research2020

Glucose Transporter-1 Cooperating with AKT Signaling Promote Gastric Cancer Progression.

Diyuan Zhou, Linhua Jiang, Lichen Jin, Yizhou Yao, Peijie Wang, Xinguo Zhu

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  5. Metabolic reprogramming and plasticity of cancer stem cells.Frontiers in cell and developmental biology · 2026
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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

6 authors at 1 institution in 1 country.

Diyuan Zhou *Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People's Republic of China.ORCID 0000-0003-4980-6796
Linhua Jiang *Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People's Republic of China.
Lichen Jin *Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People's Republic of China.
Yizhou YaoDepartment of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People's Republic of China.
Peijie WangInstitute of Mental Health, The Affiliated Guangji Hospital of Soochow University, Suzhou, Jiangsu, People's Republic of China.
Xinguo ZhuDepartment of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People's Republic of China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveHigh expression of GLUT1 has been observed in numerous solid cancers, facilitating glucose consumption for supporting tumor cell survival. The altered metabolic activity is regulated by series of signaling pathways, including AKT signaling that acts as a key role in glucose metabolism and shows close correlation with the malignant transformation. In this study, we aimed to elucidate the effect of GLUT1 on gastric cancer (GC) and to explore the relation between GLUT1 and AKT signaling. MATERIALS AND

methodsGLUT1, p-AKT, and p-S6k1 expression were investigated by immunohistochemistry and semi-quantitative analysis in 57 paired-GC samples. The relationship of GLUT1 with clinical indexes in GC tissues was investigated. The effects of GLUT1 on the prognosis of GC patients and the underlying mechanism involved were studied by subgroup analysis.

resultsIn GC tissues, an obvious increase in GLUT1 expression was observed when compared with that of normal tissues (

conclusionHigh expression of GLUT1 facilitated GC progression, leading to poor prognosis. Overexpression of GLUT1 activated AKT-S6K1 axis, resulting in adverse outcomes of GC. GLUT1 is novel indicator of GC prognosis and GLUT1 targeted metabolic treatment that has potential therapeutic value.

Indexed as

AKTgastric cancerGLUT1S6K1

Identifiers

PMID32581586
PMCPMC7276340
OpenAlexW3033550003

What OpenQuestion holds

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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.