Evidence map›Paper›PMID 37974357›Full record

ArticleCell cycle (Georgetown, Tex.)2023

Depleting ANTXR1 suppresses glioma growth via deactivating PI3K/AKT pathway.

Chaoyang Zhou, Aijun Liang, Jianzhong Zhang, Jingxing Leng, Bin Xi, Bin Zhou, Yu Yang, Ronglan Zhu, Liangchen Zhong, Xingxing Jiang and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 32% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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

11 authors at 2 institutions in 1 country.

Chaoyang Zhou
Aijun Liang
Jianzhong Zhang
Jingxing LengDepartment of Neurosurgery, Jiangxi Provincial People's Hospital the First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi Province, China.
Bin XiDepartment of Neurosurgery, Jiangxi Provincial People's Hospital the First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi Province, China.
Bin ZhouDepartment of Neurosurgery, Jiangxi Provincial People's Hospital the First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi Province, China.
Yu YangDepartment of Neurosurgery, Jiangxi Provincial People's Hospital the First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi Province, China.
Ronglan ZhuDepartment of Neurosurgery, Jiangxi Provincial People's Hospital the First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi Province, China.
Liangchen ZhongDepartment of Neurosurgery, Jiangxi Provincial People's Hospital the First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi Province, China.
Xingxing JiangDepartment of Neurosurgery, Jiangxi Provincial People's Hospital the First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi Province, China.
Dengfeng WanDepartment of Neurosurgery, Jiangxi Provincial People's Hospital the First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi Province, China.
Jiangxi Provincial People's Hospital · CNFirst Affiliated Hospital of Jiangxi Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gliomas are commonly known as primary brain tumors and associated with frequent recurrence and an unsatisfactory prognosis despite extensive research in the underlying molecular mechanisms. We aimed to examine the role of ANTXR1 in glioma tumorigenesis and explore its downstream regulatory mechanism. ANTXR1 expression in clinical specimens and its relationship with some pathological characteristics were detected using immunohistochemical staining. After silencing/upregulating ANTXR1 through lentiviral transfection in glioma cell lines, qRT-PCR and western blotting were used to examine mRNA and protein levels, and cell phenotype was also detected. ANTXR1-knockdown and -overexpression cells were then processed by AKT activator and PI3K inhibitor, respectively, to verify downstream PI3K/AKT pathway regulated by ANTXR1. Xenograft nude mice models were constructed to verify the role of ANTXR1

Indexed as

GliomaProto-Oncogene Proteins c-aktAnimalsApoptosisCarcinogenesisCell Adhesion MoleculesCell Line, TumorCell ProliferationHumansMiceMice, NudeMicrofilament ProteinsPhosphatidylinositol 3-KinasesReceptors, Cell SurfaceSignal TransductionANTXR1 protein, humanCell Adhesion MoleculesMicrofilament ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Cell SurfaceANTXR1Gliomametastasisproliferation

Identifiers

PMID37974357
PMCPMC10732648
OpenAlexW4388774168

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.