Evidence map›Paper›PMID 34047477›Full record

ArticleClinical and translational medicine2021

Glioma glycolipid metabolism: MSI2-SNORD12B-FIP1L1-ZBTB4 feedback loop as a potential treatment target.

Weiwei Dong, Xiaobai Liu, Chunqing Yang, Di Wang, Yixue Xue, Xuelei Ruan, Mengyang Zhang, Jian Song, Heng Cai, Jian Zheng and 1 more

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 53 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

11 authors at 2 institutions in 1 country.

Weiwei DongDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.
Xiaobai LiuDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.
Chunqing YangDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.
Di WangDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.
Yixue XueDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang, China.
Xuelei RuanDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang, China.
Mengyang ZhangDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang, China.
Jian SongDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.
Heng CaiDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.
Jian ZhengDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.
Yunhui LiuDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.ORCID 0000-0001-6487-8718
Shenyang Medical College · CNChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal energy metabolism, including enhanced aerobic glycolysis and lipid synthesis, is a well-established feature of glioblastoma (GBM) cells. Thus, targeting the cellular glycolipid metabolism can be a feasible therapeutic strategy for GBM. This study aimed to evaluate the roles of MSI2, SNORD12B, and ZBTB4 in regulating the glycolipid metabolism and proliferation of GBM cells. MSI2 and SNORD12B expression was significantly upregulated and ZBTB4 expression was significantly low in GBM tissues and cells. Knockdown of MSI2 or SNORD12B or overexpression of ZBTB4 inhibited GBM cell glycolipid metabolism and proliferation. MSI2 may improve SNORD12B expression by increasing its stability. Importantly, SNORD12B increased utilization of the ZBTB4 mRNA transcript distal polyadenylation signal in alternative polyadenylation processing by competitively combining with FIP1L1, which decreased ZBTB4 expression because of the increased proportion of the 3' untranslated region long transcript. ZBTB4 transcriptionally suppressed the expression of HK2 and ACLY by binding directly to the promoter regions. Additionally, ZBTB4 bound the MSI promoter region to transcriptionally suppress MSI2 expression, thereby forming an MSI2/SNORD12B/FIP1L1/ZBTB4 feedback loop to regulate the glycolipid metabolism and proliferation of GBM cells. In conclusion, MSI2 increased the stability of SNORD12B, which regulated ZBTB4 alternative polyadenylation processing by competitively binding to FIP1L1. Thus, the MSI2/SNORD12B/FIP1L1/ZBTB4 positive feedback loop plays a crucial role in regulating the glycolipid metabolism of GBM cells and provides a potential drug target for glioma treatment.

Indexed as

Brain NeoplasmsCell ProliferationGene Knockdown TechniquesGliomaGlycolipidsHEK293 CellsHumansmRNA Cleavage and Polyadenylation FactorsRepressor ProteinsRNA-Binding ProteinsRNA, Small NucleolarUp-RegulationFIP1L1 protein, humanGlycolipidsmRNA Cleavage and Polyadenylation FactorsMSI2 protein, humanRepressor ProteinsRNA-Binding ProteinsRNA, Small NucleolarZBTB4 protein, humanalternative polyadenylationgliomaglycolipid metabolismmolecular patternMSI2potential targetprediction and personalized preventionSNORD12Btranslational researchZBTB4

Identifiers

PMID34047477
PMCPMC8114150
OpenAlexW3160001579

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.