Evidence map›Paper›PMID 39149873›Full record

ArticleCancer medicine2024

NRBP1 promotes malignant phenotypes of glioblastoma by regulating PI3K/Akt activation.

Anli Zhang, Shichao Peng, Sibai Sun, Shan Ye, Ye Zhao, Qiang Wu

Abstract read
In one paragraph

Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–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

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

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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

6 authors.

Anli ZhangDepartment of Pathology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.ORCID 0000-0003-4137-2225
Shichao PengTeaching and Research Section of Nuclear Medicine, School of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Sibai SunDivision of Life Sciences and Medicine, Department of Pathology, The First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, China.
Shan YeDivision of Life Sciences and Medicine, Department of Pathology, The First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, China.
Ye ZhaoTeaching and Research Section of Nuclear Medicine, School of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Qiang WuDepartment of Pathology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.ORCID 0000-0002-8738-3723

Funding

National Natural Science Foundation of China 12275003
6 · The paper itself

Abstract

objectivesGlioblastoma (GBM) is the most aggressive of intracranial gliomas. Despite the maximal treatment intervention, the median survival rate is still about 14-16 months. Nuclear receptor-binding protein 1 (NRBP1) has a potential growth-promoting role on biology function of cells. In this study, we investigated whether NRBP1 promotes GBM malignant phenotypes and the potential mechanisms.

methodsThe correlation between NRBP1 and glioma grade, prognosis in TCGA/CGGA databases and our clinical data were analyzed. Next, we conducted knockout and overexpression of NRBP1 on GBM cells to verify that NRBP1 promoted cell proliferation, invasion, and migration in vitro and in vivo. Finally, we detected the impact of NRBP1 on PI3K/Akt signaling pathway and EMT.

resultsThere was a correlation between elevated NRBP1 expression and advanced stage glioma, as well as decreased overall and disease-free survival. The suppression of proliferation, invasion, and migration of tumor cells was observed upon NRBP1 knockout, and in vitro studies also demonstrated the induction of apoptotic cell death. Whereas, its overexpression is associated with high multiplication rate, migration, invasion, and apoptotic escape. GO enrichment and KEGG analysis revealed that NRBP1 regulated differentially expressed gene clusters are involved in PI3K/Akt signaling pathway, as well as EMT mediated by this pathway. Moreover, the effects of NRBP1 knockdown and overexpression on GBM were mitigated by MK-2206 and SC79, both of which respectively function as an inhibitor and an activator of the PI3K/Akt signaling pathway. Similarly, the suppression of NRBP1 led to a decrease in tumor growth, whereas its overexpression promoted tumor growth in a mouse model.

conclusionsThis study shows that NRBP1 promotes malignant phenotypes in GBM by activating PI3K/Akt pathway. Hence, it can function as both a predictive indicator and a new target for therapies in GBM treatment.

Indexed as

Brain NeoplasmsCell MovementCell ProliferationGlioblastomaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAnimalsApoptosisCell Line, TumorEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceNRBP1 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Cytoplasmic and NuclearVesicular Transport Proteinsepithelial‐mesenchymal transitionglioblastomanuclear receptor‐binding protein 1PI3K/Akt signaling pathwaypseudokinase

Identifiers

PMID39149873
PMCPMC11327863

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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.