Evidence map›Paper›PMID 31772693›Full record

ArticleDisease markers2019

Identification of Key Pathways and Genes in the Orai2 Mediated Classical and Mesenchymal Subtype of Glioblastoma by Bioinformatic Analyses.

Feng Yuan, Li Yi, Long Hai, Yingshuai Wang, Yihan Yang, Tao Li, Luqing Tong, Haiwen Ma, Peidong Liu, Haolang Ming and 4 more

Abstract read
In one paragraph

Article in Disease markers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Receptor Tyrosine Kinase Signaling and Targeting in Glioblastoma Multiforme.International journal of molecular sciences · 2021
    Review
  4. Review
  5. Article
  6. 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

14 authors.

Feng YuanDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.ORCID https://orcid.org/0000-0002-8132-9224
Li YiDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Long HaiThe First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, China.
Yingshuai WangDepartment of Internal Medicine III, University Hospital Munich, Ludwig-Maximilians-University, Munich, Germany.
Yihan YangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Tao LiDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Luqing TongDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Haiwen MaDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Peidong LiuDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Haolang MingDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Bingcheng RenDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Shengping YuDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Yu LinDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Xuejun YangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, China.ORCID https://orcid.org/0000-0001-7056-1223

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCa

methodsVia The Cancer Genome Atlas (TCGA), French, Sun, and Gene Expression Omnibus (GEO) (GDS3885) datasets, we collected 1231 cases with RNA-seq data and analyzed the functional annotation of Orai2 by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Univariate and multivariate survival analyses were applied to 823 patients with survival data.

resultsWe discovered that Orai2 was markedly upregulated in GBM compared to normal brain samples and lower-grade gliomas (LGG). Survival analysis found that higher expression of Orai2 was independently associated with a worse prognosis of patients with the classical and mesenchymal subtypes of GBM. Simultaneously, Orai2 expression was higher in tumors of the classical and mesenchymal subtypes than other subtypes and was significantly correlated with classical- and mesenchymal-related genes. GO and KEGG pathway analysis revealed that genes significantly correlated with Orai2 were involved in the JNK pathway. Through screening transcriptomic data, we found a strong association between Orai2 and apoptosis, stemness, and an epithelial-mesenchymal transition- (EMT-) like phenotype.

conclusionAs a prognostic factor, Orai2 is obviously activated in the classical and mesenchymal subtypes of GBM and promotes glioma cell self-renewal, apoptosis, and EMT-like by the JNK pathway. These findings indicate that Orai2 could be a candidate prognostic and therapeutic target, especially for the classical and mesenchymal subtypes of GBM.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBiomarkers, TumorBrain NeoplasmsCluster AnalysisDatabases, FactualEpithelial-Mesenchymal TransitionGlioblastomaHumansKaplan-Meier EstimateMAP Kinase Signaling SystemOligonucleotide Array Sequence AnalysisORAI2 ProteinPrognosisBiomarkers, TumorORAI2 ProteinORAI2 protein, human

Identifiers

PMID31772693
PMCPMC6855003

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.