Evidence map›Paper›PMID 34536269›Full record

ArticleAging2021

LHX9, a p53-binding protein, inhibits the progression of glioma by suppressing glycolysis.

Xiangying Luo, Jianwei Ge, Tao Chen, Jinfang Liu, Ziyuan Liu, Changlong Bi, Song Lan

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

7 citing papers in PubMed, 31 citations in OpenAlex.

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  6. Expression analysis of human glioma susceptibility gene andAnnals of translational medicine · 2023
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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 4 institutions in 1 country.

Xiangying LuoDepartment of Neurosurgery, XiangYa Hospital of Central South University, Changsha 410078, P.R. China.
Jianwei GeDepartment of Neurosurgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, P.R. China.
Tao ChenDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, P.R. China.
Jinfang LiuDepartment of Neurosurgery, XiangYa Hospital of Central South University, Changsha 410078, P.R. China.
Ziyuan LiuDepartment of Neurosurgery, XiangYa Hospital of Central South University, Changsha 410078, P.R. China.
Changlong BiDepartment of Neurosurgery, XiangYa Hospital of Central South University, Changsha 410078, P.R. China.
Song LanDepartment of Neurosurgery, XiangYa Hospital of Central South University, Changsha 410078, P.R. China.
Central South University · CNXiangya Hospital Central South University · CNFirst Affiliated Hospital of Guangzhou Medical University · CNRenji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeLHX9 methylation has been reported in many tumors, but its functions and related mechanisms in glioma are still unknown and need to be verified.

methodsThe protein level of LHX9 in glioma tissues was examined using western blotting and immunohistochemistry, and the functions of LHX9 in glioma cell lines were investigated using MTT and colony formation assays. In addition, the interaction between LHX9 and P53 was analyzed by immunoprecipitation, and the roles of LHX9 in cancer metabolism were explored by measuring metabolites.

resultsIn this study, we found that the LHX9 expression level was decreased in glioma specimens, and the upregulation of LHX9 expression inhibited the growth of glioma cells in liquid medium and on soft agar. Regarding the molecular mechanism, we found that LHX9 interacted with p53, and downregulation of LHX9 promoted the expression of the glycolysis-related enzyme PGK1 and increased the lactic acid content. By interfering with the expression of LHX9, the tumorigenicity of glioma cells was promoted, an outcome blocked by further interference with PGK1 expression.

conclusionIn summary, the decreased expression of LHX9 in gliomas activates the expression of the glycolysis-related enzyme PGK1, thereby promoting the development of gliomas, suggesting that the LHX9-PGK1 signaling axis can be used as a target for the treatment of glioma.

Indexed as

GlycolysisAnimalsApoptosisBrain NeoplasmsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGliomaHumansLIM-Homeodomain ProteinsMaleMiceMice, NudeProtein BindingSignal TransductionTranscription FactorsLHX9 protein, humanLIM-Homeodomain ProteinsTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53gliomaglycolysisLHX9p53PGK1

Identifiers

PMID34536269
PMCPMC8507291
OpenAlexW3199323442

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LicenceCC BY
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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.