Evidence map›Paper›PMID 28767320›Full record

ArticleCell cycle (Georgetown, Tex.)2017

Forkhead Box M1 positively regulates UBE2C and protects glioma cells from autophagic death.

Liang Guo, Zhiming Ding, Nunu Huang, Zhengsong Huang, Nu Zhang, Zhibo Xia

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  6. Review
  7. Article
  8. Role of UBE2C in Brain Cancer Invasion and Dissemination.International journal of molecular sciences · 2023
    Review
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  10. Article
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  12. Genes · 2022
    Article
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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 2 institutions in 1 country.

Liang Guoa Department of Neurosurgery , The First Affiliated Hospital of Sun Yat-sen University , Guangzhou , Guangdong Province , China.
Zhiming Dinga Department of Neurosurgery , The First Affiliated Hospital of Sun Yat-sen University , Guangzhou , Guangdong Province , China.
Nunu Huanga Department of Neurosurgery , The First Affiliated Hospital of Sun Yat-sen University , Guangzhou , Guangdong Province , China.
Zhengsong Huanga Department of Neurosurgery , The First Affiliated Hospital of Sun Yat-sen University , Guangzhou , Guangdong Province , China.
Nu Zhanga Department of Neurosurgery , The First Affiliated Hospital of Sun Yat-sen University , Guangzhou , Guangdong Province , China.
Zhibo Xiaa Department of Neurosurgery , The First Affiliated Hospital of Sun Yat-sen University , Guangzhou , Guangdong Province , China.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ubiquitin-conjugating enzyme E2C (UBE2C) is characterized as a crucial molecule in cancer cell growth that plays an essential role in the development of gliomas, but the detailed mechanisms have not been fully elucidated. In this study, we found that Forkhead box transcription factor M1 (FoxM1) overexpression increased UBE2C expression, whereas FoxM1 suppression inhibited UBE2C expression in glioma cells. In addition, high FoxM1/UBE2C expression was significantly correlated with poor prognosis in glioma. We subsequently demonstrated that UBE2C was a direct transcriptional target of FoxM1, and site-directed mutations markedly down-regulated UBE2C promoter activity. Moreover, UBE2C siRNA (si-UBE2C) significantly induced glioma cell autophagy and increased both mCherry-LC3 punctate fluorescence and LC3B-II/LC3-I expression. Notably, the si-UBE2C-induced decrease in cell viability was markedly inhibited by the autophagy inhibitor bafilomycin A1. The silencing of UBE2C resulted in a distinct inhibition of the PI3K-Akt-mTOR pathway, which functions in the negative modulation of autophagy. Collectively, our findings provide clinical and molecular evidence that FoxM1 promotes glioma progression by enhancing UBE2C transcription and that the inhibition of UBE2C partially induces autophagic glioma cell death. Thus, targeting the FoxM1-UBE2C axis has therapeutic potential in the treatment of gliomas.

Indexed as

AutophagyNeuroprotectionAdolescentAdultApoptosisBrain NeoplasmsCell Line, TumorCell SurvivalComputational BiologyFemaleForkhead Box Protein M1Gene Knockdown TechniquesGene SilencingGliomaHumansKaplan-Meier Estimatebafilomycin A1Forkhead Box Protein M1MacrolidesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesUBE2C protein, humanUbiquitin-Conjugating EnzymesautophagyFoxM1gliomatranscriptionUBE2C

Identifiers

PMID28767320
PMCPMC5602297
OpenAlexW2739652862

What OpenQuestion holds

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LicenceCC BY
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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.