Evidence map›Paper›PMID 33723235›Full record

ArticleCell death & disease2021

NIK promotes metabolic adaptation of glioblastoma cells to bioenergetic stress.

Michael L Kamradt, Ji-Ung Jung, Kathryn M Pflug, Dong W Lee, Victor Fanniel, Raquel Sitcheran

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

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  14. Dysregulated inter-mitochondrial crosstalk in glioblastoma cells revealed by in situ cryo-electron tomography.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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 at 1 institution in 1 country.

Michael L Kamradt *Department of Molecular & Cellular Medicine, Texas A&M University Health Science Center, College Station, TX, 77845, USA.ORCID http://orcid.org/0000-0002-0628-1988
Ji-Ung Jung *Department of Molecular & Cellular Medicine, Texas A&M University Health Science Center, College Station, TX, 77845, USA.
Kathryn M PflugDepartment of Molecular & Cellular Medicine, Texas A&M University Health Science Center, College Station, TX, 77845, USA.
Dong W LeeDepartment of Molecular & Cellular Medicine, Texas A&M University Health Science Center, College Station, TX, 77845, USA.
Victor FannielDepartment of Molecular & Cellular Medicine, Texas A&M University Health Science Center, College Station, TX, 77845, USA.
Raquel SitcheranDepartment of Molecular & Cellular Medicine, Texas A&M University Health Science Center, College Station, TX, 77845, USA. sitcheran@tamu.edu.ORCID http://orcid.org/0000-0001-8916-9707
Texas A&M Health Science Center · US

Funding

Pathway-Specific NF-kappaB Regulatory Networks in GliomaR01NS082554 · NINDS · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI SITCHERAN, RAQUEL · 2014 to 2022
$2.5M
NINDS NIH HHS R01 NS082554
6 · The paper itself

Abstract

Cancers, including glioblastoma multiforme (GBM), undergo coordinated reprogramming of metabolic pathways that control glycolysis and oxidative phosphorylation (OXPHOS) to promote tumor growth in diverse tumor microenvironments. Adaptation to limited nutrient availability in the microenvironment is associated with remodeling of mitochondrial morphology and bioenergetic capacity. We recently demonstrated that NF-κB-inducing kinase (NIK) regulates mitochondrial morphology to promote GBM cell invasion. Here, we show that NIK is recruited to the outer membrane of dividing mitochondria with the master fission regulator, Dynamin-related protein1 (DRP1). Moreover, glucose deprivation-mediated metabolic shift to OXPHOS increases fission and mitochondrial localization of both NIK and DRP1. NIK deficiency results in decreased mitochondrial respiration, ATP production, and spare respiratory capacity (SRC), a critical measure of mitochondrial fitness. Although IκB kinase α and β (IKKα/β) and NIK are required for OXPHOS in high glucose media, only NIK is required to increase SRC under glucose deprivation. Consistent with an IKK-independent role for NIK in regulating metabolism, we show that NIK phosphorylates DRP1-S616 in vitro and in vivo. Notably, a constitutively active DRP1-S616E mutant rescues oxidative metabolism, invasiveness, and tumorigenic potential in NIK

Indexed as

Energy MetabolismBrain NeoplasmsCell Line, TumorDynaminsGene Expression Regulation, NeoplasticGlioblastomaHumansMitochondriaMitochondrial DynamicsMitochondrial MembranesNF-kappaB-Inducing KinasePhosphorylationProtein Serine-Threonine KinasesTumor MicroenvironmentDNM1L protein, humanDynaminsNF-kappaB-Inducing KinaseProtein Serine-Threonine Kinases

Identifiers

PMID33723235
PMCPMC7960998
OpenAlexW3138011429

What OpenQuestion holds

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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.