Evidence map›Paper›PMID 33119597›Full record

ArticlePloS one2020

Identification of driver genes and key pathways of non-functional pituitary adenomas predicts the therapeutic effect of STO-609.

Bo Wu, Shanshan Jiang, Xinhui Wang, Sheng Zhong, Yiming Bi, Dazhuang Yi, Ge Liu, Fangfei Hu, Gaojing Dou, Yong Chen and 2 more

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

Article in PloS one, 2020. 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
0.1field-weighted citation impact, top 46% 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. 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 5 institutions in 1 country.

Bo WuClinical College, Jilin University, Changchun, China.
Shanshan JiangInstitute of Zoology, China Academy of Science, Beijing, China.
Xinhui WangClinical College, Jilin University, Changchun, China.
Sheng ZhongDepartment of Neurosurgery, Cancer Hospital of Sun Yat sen University, Guangzhou, China.
Yiming BiDepartment of Neurosurgery, The First Bethune Hospital of Jilin University, Changchun, China.
Dazhuang YiDepartment of Neurosurgery, The First Bethune Hospital of Jilin University, Changchun, China.
Ge LiuCollege of Pharmacy, Jilin University, Changchun, China.
Fangfei HuCollege of Pharmacy, Jilin University, Changchun, China.
Gaojing DouClinical College, Jilin University, Changchun, China.
Yong ChenDepartment of Neurosurgery, The First Bethune Hospital of Jilin University, Changchun, China.ORCID 0000-0003-3394-6516
Yi WuDepartment of Neurosurgy, Jiangmen Central Hospital, Jiangmen, China.
Jiajun DongDepartment of Neurosurgy, Jiangmen Central Hospital, Jiangmen, China.
Jilin University · CNFirst Bethune Hospital of Jilin University · CNJiangmen Central Hospital · CNInstitute of Zoology · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveOur study is to identify DEGs (Differentially Expressed Genes), comprehensively investigate hub genes, annotate enrichment functions and key pathways of Non-functional pituitary adenomas (NFPAs), and also to verify STO-609 therapeutic effect.

methodsThe gene expression level of NFPA and normal tissues were compared to identify the DEGs (Differential expressed genes) based on gene expression profiles (GSE2175, GSE26966 and GSE51618). Enrichment functions, pathways and key genes were identified by carrying out GO (Gene Ontology), KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis and PPI (Protein-Protein Interation) network analysis. Moreover, experiments in vitro were conducted to verify the anti-NFPAs effects of STO-609.

results169 over-expression genes and 182 low expression genes were identified among 3 datasets. Dopaminergic synapse and vibrio cholerae infection pathways have distinctly changed in NFPA tissues. The Ca2+/CaM pathway played important roles in NFPA. Four hub proteins encoded by genes CALM1, PRDM10, RIPK4 and MAD2L1 were recognized as hub proteins. In vitro, assays showed that STO-609 induced apoptosis of NFPA cells to inhibit the hypophysoma cellular viability, diffusion and migration.

conclusionFour hub proteins, encoded by gene CALM1, PRDM10, RIPK4 and MAD2L1, played important roles in NFPA development. The Ca2+/CaM signaling pathway had significant alternations during NFPA forming process, the STO-609, a selective CaM-KK inhibitor, inhibited NFPA cellular viability, proliferation and migration. Meanwhile, NFPA was closely related to parkinson's disease (PD) in many aspects.

Indexed as

AnimalsAntineoplastic AgentsBenzimidazolesCalcium-Calmodulin-Dependent Protein Kinase KinaseCell Line, TumorComputational BiologyGene Expression ProfilingGene OntologyHumansMiceMicroarray AnalysisNaphthalimidesPituitary NeoplasmsProtein Kinase InhibitorsSignal TransductionAntineoplastic AgentsBenzimidazolesCalcium-Calmodulin-Dependent Protein Kinase KinaseNaphthalimidesProtein Kinase InhibitorsSTO 609

Identifiers

PMID33119597
PMCPMC7595405
OpenAlexW3096183836

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.