Evidence map›Paper›PMID 25926381›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015

Genetic and molecular analyses reveal G6PC as a key element connecting glucose metabolism and cell cycle control in ovarian cancer.

Ting Guo, Tao Chen, Chao Gu, Bin Li, Congjian Xu

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Interplay Between Glucose Metabolism and Chromatin Modifications in Cancer.Frontiers in cell and developmental biology · 2021
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  10. [Glucose-6 phosphatase catalytic subunit inhibits the proliferation of liver cancer cells by inducing cell cycle arrest].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022
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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

5 authors at 1 institution in 1 country.

Ting GuoDepartment of Gynaecology, Obstetrics and Gynaecology Hospital, Fudan University, Shanghai, 200011, People's Republic of China.
Tao ChenDepartment of Stem Cell and and Regenerative Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA, 02138, USA.
Chao GuDepartment of Gynaecology, Obstetrics and Gynaecology Hospital, Fudan University, Shanghai, 200011, People's Republic of China.
Bin LiDepartment of Gynaecology, Obstetrics and Gynaecology Hospital, Fudan University, Shanghai, 200011, People's Republic of China.
Congjian XuDepartment of Gynaecology, Obstetrics and Gynaecology Hospital, Fudan University, Shanghai, 200011, People's Republic of China. drxucongjian@163.com.
Harvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We aimed to evaluate the role of glucose-6-phosphatase, catalytic subunit (G6PC) in ovarian cancer and to exploit its therapeutic potential. With reproduction of The Cancer Genome Atlas (TCGA) database, we studied expressions of genes in the glucose metabolism pathways in silico. The cBioPortal For Cancer Genomics was used to study the clinical, pathological and molecular profiles of G6PC. In vitro studies were performed to validate the function of G6PC and the effect of genetic and pharmaceutical G6PC inhibition. In 158 ovarian cancer (OvCa) patients with complete RNA-seq data, G6PC expression was increased in 27 patients (17 %). Both overall survival (OS) and disease-free period were significantly shorter in cases with increased G6PC level. Significantly decreased total and phosphorylated CDKN1B level was noted in OvCa with increased G6PC expression. Silenced G6PC in OvCa cells induced decreased cell proliferation, viability, invasiveness and anchorage-independent cell growth. G6PC silencing also induced enhanced cell cycle control proteins and restoration of CDKN1B level. Pharmaceutical inhibition of G6PC with specific compound showed similar effects to genetic silencing. G6PC played dual roles both in glucose metabolism and cell cycle control in OvCa, which potentiated it a promising therapeutic target.

Indexed as

Catalytic DomainCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p27Disease-Free SurvivalFemaleGene Expression Regulation, NeoplasticGene SilencingGlucoseGlucose-6-PhosphataseHumansOvarian NeoplasmsPhosphorylationCDKN1B protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p27GlucoseGlucose-6-PhosphataseCDKN1BCell cycleG6PCGlucose metabolismOvarian cancer

Identifiers

PMID25926381
OpenAlexW2063398467

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.