Evidence map›Paper›PMID 29896817›Full record

ArticleCancer science2018

CDK2 positively regulates aerobic glycolysis by suppressing SIRT5 in gastric cancer.

Zhenyong Tang, Lei Li, Yuntian Tang, Dongyi Xie, Kun Wu, Weiyuan Wei, Qiang Xiao

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

49 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
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  6. World journal of gastrointestinal oncology · 2025
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  15. Energy metabolism: a new target for gastric cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review
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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

7 authors at 3 institutions in 1 country.

Zhenyong TangDepartment of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.ORCID http://orcid.org/0000-0001-6348-8427
Lei LiDepartment of Surgery, People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Yuntian TangDepartment of Surgery, People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Dongyi XieDepartment of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Kun WuDepartment of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Weiyuan WeiDepartment of Gastrointestinal Surgery, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, China.
Qiang XiaoDepartment of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Guangxi Medical University · CNThe People's Hospital of Guangxi Zhuang Autonomous Region · CNTumor Hospital of Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although significant progress has been made in the diagnosis and treatment of gastric cancer, the overall survival rate of the disease remains unchanged at approximately 20%-25%. Thus, there is an urgent need for a better understanding of the molecular biology aspects of the disease in the hope of discovering novel diagnosis and treatment strategies. Recent years have witnessed decisive roles of aberrant cancer cell metabolism in the maintenance of malignant hallmarks of cancers, and cancer cell metabolism has been regarded as a novel target for the treatment of cancer. CDK2, a cell cycle-dependent kinase that usually regulates cell cycle progression and the DNA damage response, is reported to be upregulated in many cancers. However, little is known about its role in cancer cell metabolism. In the present study, we showed that silencing CDK2 inhibited the aerobic glycolytic capacity of gastric cancer cell lines. Mechanism explorations showed that silencing CDK2 increased expression of the SIRT5 tumor suppressor. In addition, the physiological roles of SIRT5 in the regulation of proliferation and glycolysis were studied in gastric cancer cells. Taken together, the present study uncovered novel roles of the CDK2/SIRT5 axis in gastric cancer and suggests future studies concerning gastric cancer cell metabolism.

Indexed as

Cell CycleCell Line, TumorCell ProliferationCyclin-Dependent Kinase 2DNA DamageGlycolysisHumansSirtuinsStomach NeoplasmsSurvival RateUp-RegulationCDK2 protein, humanCyclin-Dependent Kinase 2SIRT5 protein, humanSirtuinsCDK2CDK2/SIRT5gastric cancerglycolysisSIRT5

Identifiers

PMID29896817
PMCPMC6113437
OpenAlexW2807926991

What OpenQuestion holds

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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.