Evidence map›Paper›PMID 33804169›Full record

ArticleInternational journal of molecular sciences2021

Dual Specificity Kinase DYRK3 Promotes Aggressiveness of Glioblastoma by Altering Mitochondrial Morphology and Function.

Kyeongmin Kim, Sungmin Lee, Hyunkoo Kang, Eunguk Shin, Hae Yu Kim, HyeSook Youn, BuHyun Youn

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

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  11. Oncogenic Gαq activates RhoJ through PDZ-RhoGEF.International journal of molecular sciences · 2023
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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

7 authors at 3 institutions in 1 country.

Kyeongmin KimDepartment of Integrated Biological Science, Pusan National University, Busan 46241, Korea.
Sungmin LeeDepartment of Integrated Biological Science, Pusan National University, Busan 46241, Korea.
Hyunkoo KangDepartment of Integrated Biological Science, Pusan National University, Busan 46241, Korea.
Eunguk ShinDepartment of Integrated Biological Science, Pusan National University, Busan 46241, Korea.
Hae Yu KimDepartment of Neurosurgery, Haeundae Paik Hospital, Inje University College of Medicine, Busan 48108, Korea.
HyeSook YounDepartment of Integrative Bioscience and Biotechnology, Sejong University, Seoul 05006, Korea.
BuHyun YounDepartment of Integrated Biological Science, Pusan National University, Busan 46241, Korea.
Pusan National University · KRInje University Haeundae Paik Hospital · KRSejong University · KR

Funding

Ministry of Science and ICT, South Korea 2020M2D9A2094156National Research Foundation of Korea NRF-2019R1A2C1008051National Research Foundation of Korea NRF-2020R1A2C2005793
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is a malignant primary brain tumor with poor patient prognosis. Although the standard treatment of GBM is surgery followed by chemotherapy and radiotherapy, often a small portion of surviving tumor cells acquire therapeutic resistance and become more aggressive. Recently, altered kinase expression and activity have been shown to determine metabolic flux in tumor cells and metabolic reprogramming has emerged as a tumor progression regulatory mechanism. Here we investigated novel kinase-mediated metabolic alterations that lead to acquired GBM radioresistance and malignancy. We utilized transcriptomic analyses within a radioresistant GBM orthotopic xenograft mouse model that overexpresses the dual specificity tyrosine-phosphorylation-regulated kinase 3 (DYRK3). We find that within GBM cells, radiation exposure induces DYRK3 expression and DYRK3 regulates mammalian target of rapamycin complex 1 (mTORC1) activity through phosphorylation of proline-rich AKT1 substrate 1 (PRAS40). We also find that DYRK3 knockdown inhibits dynamin-related protein 1 (DRP1)-mediated mitochondrial fission, leading to increased oxidative phosphorylation (OXPHOS) and reduced glycolysis. Importantly, enforced DYRK3 downregulation following irradiation significantly impaired GBM cell migration and invasion. Collectively, we suggest DYRK3 suppression may be a novel strategy for preventing GBM malignancy through regulating mitochondrial metabolism.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell Line, TumorCell ProliferationDynaminsGene Expression Regulation, NeoplasticGlioblastomaHumansMiceMitochondriaOxidative PhosphorylationProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktRadiation ToleranceXenograft Model Antitumor AssaysAdaptor Proteins, Signal TransducingAKT1 protein, humanAKT1S1 protein, humanDNM1L protein, humanDynaminsDYRK3 protein, humanProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktDYRK3glioblastoma multiformemitochondrial fissionradioresistance

Identifiers

PMID33804169
PMCPMC8000785
OpenAlexW3137558542

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.