Evidence map›Paper›PMID 38491378›Full record

ArticleJournal of translational medicine2024

Hypoxia promotes metastasis by relieving miR-598-3p-restricted glycolysis in gastric cancer.

Wei Zhou, Mengyuan Tang, Dan He, Yi Shen, Ziwei Huang, Wenxin Xia, Zhiyun Wu, Wenxiang Wei, Hui Zheng, Qi Wang and 2 more

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

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Review
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

12 authors at 1 institution in 1 country.

Wei Zhou *Department of Clinical Laboratory, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China.
Mengyuan Tang *Department of Clinical Laboratory, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China.
Dan HeDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China.
Yi ShenDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China.
Ziwei HuangDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China.
Wenxin XiaDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China.
Zhiyun WuDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China.
Wenxiang WeiDepartment of Cell Biology, Soochow University, SuZhou, 215004, Jiangsu, China.
Hui ZhengDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China.
Qi WangDepartment of Biological Treatment, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China. wangqi88@suda.edu.cn.
Weifeng ShiDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China. swf67113@163.com.
Jingting JiangDepartment of Biological Treatment, The Third Affiliated Hospital of Soochow University, ChangZhou, 213003, Jiangsu, China. jiangjingting@suda.edu.cn.ORCID 0000-0002-3128-9762
Soochow University · CN

Funding

Changzhou Sci&Tech Program CJ20210141Changzhou Sci&Tech Program CJ20220107Funding from Young Talent Development Plan of Changzhou Health Commission CZQM2020001Funding from Young Talent Development Plan of Changzhou Health Commission CZQM2020018Health and Family Planning Commission for Yang Technology talents of ChangZhou QN202103National Natural Science Foundation of China 82102473Postdoctoral Science Foundation of China 2018M632360Postgraduate Research & Practice Innovation Program of Jiangsu Province (KYCX22_3210
6 · The paper itself

Abstract

The activation of glycolysis, particularly in the context of reprogrammed energy metabolism, is increasingly recognized as a significant characteristic of cancer. However, the precise mechanisms by which glycolysis is promoted in metastatic gastric cancer cells under normal oxygen conditions remain poorly understood. MicroRNAs (miRNAs) play a crucial role in the development of malignant phenotypes in gastric cancer. Nevertheless, our understanding of the specific involvement of miRNAs in hypoxia-induced metabolic shifting and the subsequent metastatic processes is limited. Hypoxia-induced downregulation of miR-598-3p mechanistically leads to the upregulation of RMP and IGF1r, thereby promoting glycolysis. Either overexpression of miR-598-3p or R406 treatment effectively suppresses the metastasis of gastric cancer cells both in vitro and in vivo. Collectively, the depletion of miR-598-3p alters glucose metabolism from oxidative phosphorylation to glycolysis, thereby exacerbating the malignancy of gastric cancer cells. The present findings indicate a potential target for the development of therapeutics against gastric cancers with increased miR-598-3p expression.

Indexed as

MicroRNAsStomach NeoplasmsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGlycolysisHumansHypoxiaMicroRNAsMIRN-598 microRNA, humanGastric cancerGlucose metabolismHypoxiaMetastasismicroRNAs

Identifiers

PMID38491378
PMCPMC10943772
OpenAlexW4392847634

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.