Evidence map›Paper›PMID 31444412›Full record

ArticleOncogene2020

Decreased FBP1 expression rewires metabolic processes affecting aggressiveness of glioblastoma.

Beomseok Son, Sungmin Lee, Hyunwoo Kim, Hyunkoo Kang, Jaewan Jeon, Sunmi Jo, Ki Moon Seong, Su-Jae Lee, HyeSook Youn, BuHyun Youn

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

37 citing papers in PubMed, 55 citations in OpenAlex.

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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

10 authors at 5 institutions in 1 country.

Beomseok Son *Department of Integrated Biological Science, Pusan National University, Busan, 46241, Republic of Korea.
Sungmin Lee *Department of Integrated Biological Science, Pusan National University, Busan, 46241, Republic of Korea.
Hyunwoo KimDepartment of Integrated Biological Science, Pusan National University, Busan, 46241, Republic of Korea.
Hyunkoo KangDepartment of Integrated Biological Science, Pusan National University, Busan, 46241, Republic of Korea.
Jaewan JeonDepartment of Integrated Biological Science, Pusan National University, Busan, 46241, Republic of Korea.
Sunmi JoDepartment of Radiation Oncology, Haeundae Paik Hospital, Inje University School of Medicine, Busan, 48108, Republic of Korea.
Ki Moon SeongLaboratory of Low Dose Risk Assessment, National Radiation Emergency Medical Center, Korea Institute of Radiological & Medical Sciences, Seoul, 01812, Republic of Korea.
Su-Jae LeeDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, 04763, Republic of Korea.
HyeSook YounDepartment of Integrative Bioscience and Biotechnology, Sejong University, Seoul, 05006, Republic of Korea.
BuHyun YounDepartment of Integrated Biological Science, Pusan National University, Busan, 46241, Republic of Korea. bhyoun72@pusan.ac.kr.
Pusan National University · KRInje University Haeundae Paik Hospital · KRHanyang University · KRKorea Institute of Radiological and Medical Sciences · KRSejong University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiotherapy is a standard treatment option for patients with glioblastoma (GBM). Although it has high therapeutic efficacy, some proportion of the tumor cells that survive after radiotherapy may cause side effects. In this study, we found that fructose 1,6-bisphosphatase 1 (FBP1), a rate-limiting enzyme in gluconeogenesis, was downregulated upon treatment with ionizing radiation (IR). Ets1, which was found to be overexpressed in IR-induced infiltrating GBM, was suggested to be a transcriptional repressor of FBP1. Furthermore, glucose uptake and extracellular acidification rates were increased upon FBP1 downregulation, which indicated an elevated glycolysis level. We found that emodin, an inhibitor of phosphoglycerate mutase 1 derived from natural substances, significantly suppressed the glycolysis rate and IR-induced GBM migration in in vivo orthotopic xenograft mouse models. We propose that the reduced FBP1 level reprogrammed the metabolic state of GBM cells, and thus, FBP1 is a potential therapeutic target regulating GBM metabolism following radiotherapy.

Indexed as

AnimalsCell Line, TumorFructose-BisphosphataseGene Expression Regulation, NeoplasticGlioblastomaGluconeogenesisGlucoseGlycolysisHumansMiceXenograft Model Antitumor AssaysFBP1 protein, humanFructose-BisphosphataseGlucose

Identifiers

PMID31444412
OpenAlexW2969629031

What OpenQuestion holds

Textmetadata
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.