Evidence map›Paper›PMID 39730581›Full record

ArticleScientific reports2024

The dual role of calnexin on malignant progression and tumor microenvironment in glioma.

Wenxia Wang, Yinmin Shi, Bo Yan, Yuang Cai, Han Zheng, Yuan Zhang, Liang Wang, Huijuan Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Wenxia Wang *National Engineering Research Center for Miniaturized Detection Systems, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.
Yinmin Shi *National Engineering Research Center for Miniaturized Detection Systems, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.
Bo YanNational Engineering Research Center for Miniaturized Detection Systems, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.
Yuang CaiKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Northwest University, Xi'an, 710069, Shaanxi, China.
Han ZhengNational Regional Children's Medical Center (Northwest), Xi'an Children's Hospital, Affiliated Children's Hospital of Xi'an Jiaotong University, No. 69, Xijuyuan Lane, Xi'an, 710003, China.
Yuan ZhangProvincial Key Laboratory of Biotechnology of Shaanxi Province, Northwest University, Xi'an, China.
Liang WangDepartment of Neurosurgery, Tangdu Hospital of Air Force Medical University, Xi'an, China.
Huijuan WangNational Engineering Research Center for Miniaturized Detection Systems, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China. whj@nwu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is the most common malignant brain tumor. Previous studies have reported that calnexin (CANX) is significantly up-regulated in a variety of malignant tumors, including glioma, but its biological function and mechanism in glioma is still unclear. In this study, differentially expressed proteins in 3 primary glioblastoma multiforme (GBM) tissues and 3 paracancer tissues were identified by liquid chromatography-tandem mass spectrometry-based proteomic and bioinformatic analysis. The biological function and molecular mechanism of CANX were studied in glioma cell lines (T98G and A172) by CCK-8 assay, matrigel invasion assay, wound healing assay, flow cytometry and so on. Bioinformatics methods were used to analyze the immune microenvironment of glioma patients in TCGA database, and single cell sequencing data of 8 cases of untreated primary GBM in GEO database were analyzed. Proteomic analysis found that CANX was significantly overexpressed in glioma tissues comparing with paracancer tissues. The data from TCGA validated this result and showed that CANX was associated with poor prognosis of patients. A series of experiments at the cellular level found that CANX overexpression significantly enhanced the proliferation, migration and invasion ability of GBM cells, whereas CANX silencing had opposite effects. Further research found this effect may be mediated through the activation of the PI3K/AKT/mTOR signaling. In addition, immune infiltration analysis found that CANX high-expression glioma tissues exhibited fewer CD8

Indexed as

Brain NeoplasmsGliomaTumor MicroenvironmentCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticGlioblastomaHumansMalePhosphatidylinositol 3-KinasesPrognosisProteomicsProto-Oncogene Proteins c-aktPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCalnexinGliomaPI3K/AKT/mTORTumor immune microenvironment

Identifiers

PMID39730581
PMCPMC11680814

What Socratic holds

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Registered trials

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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 Socratic graph.