Evidence map›Paper›PMID 32814835›Full record

ArticleBritish journal of cancer2020

E2F7-EZH2 axis regulates PTEN/AKT/mTOR signalling and glioblastoma progression.

Rui Yang, Mei Wang, Guanghui Zhang, Yonghua Bao, Yanan Wu, Xiuxiu Li, Wancai Yang, Hongjuan Cui

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 68 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 123 citations in OpenAlex.

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  10. E2F7 targets S100A2 to suppress CD8Journal of molecular medicine (Berlin, Germany) · 2026
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8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Rui Yang *Key Laboratory of Precision Oncology of Shandong Higher Education, Institute of Precision Medicine, Jining Medical University, Jining, China. simply_yang@126.com.ORCID http://orcid.org/0000-0002-0525-1728
Mei Wang *State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Guanghui ZhangState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Yonghua BaoKey Laboratory of Precision Oncology of Shandong Higher Education, Institute of Precision Medicine, Jining Medical University, Jining, China.
Yanan WuState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Xiuxiu LiDepartment of Pharmacy, The Second People's Hospital of Liaocheng, Liaocheng, China.
Wancai YangKey Laboratory of Precision Oncology of Shandong Higher Education, Institute of Precision Medicine, Jining Medical University, Jining, China.
Hongjuan CuiState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China. hcui@swu.edu.cn.
Southwest University · CNFourth People's Hospital of Liaocheng · CNJining Medical University · CNUniversity of Illinois Chicago · US

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81602479National Natural Science Foundation of China (National Science Foundation of China) 81672502
6 · The paper itself

Abstract

backgroundE2F transcription factors are considered to be important drivers of tumour growth. E2F7 is an atypical E2F factor, and its role in glioblastoma remains undefined.

methodsE2F7 expression was examined in patients by IHC and qRT-PCR. The overall survival probability was determined by statistical analyses. MTT assay, colony formation, cell-cycle assay, cell metastasis and the in vivo model were employed to determine the functional role of E2F7 in glioblastoma. Chromatin immunoprecipitation, luciferase assay and western blot were used to explore the underlying mechanisms.

resultsE2F7 was found to be up-regulated in glioblastoma patients, and high E2F7 expression was associated with poor overall survival in glioblastoma patients. Functional studies showed that E2F7 promoted cell proliferation, cell-cycle progression, cell metastasis and tumorigenicity abilities in vitro and in vivo. E2F7 promoted the transcription of EZH2 by binding to its promoter and increased H3K27me3 level. EZH2 recruited H3K27me3 to the promoter of PTEN and inhibited PTEN expression, and then activated the AKT/mTOR signalling pathway. In addition, restored expression of EZH2 recovered the abilities of cell proliferation and metastasis in E2F7-silencing cells.

conclusionCollectively, our findings indicate that E2F7 promotes cell proliferation, cell metastasis and tumorigenesis via EZH2-mediated PTEN/AKT/mTOR pathway in glioblastoma.

Indexed as

AnimalsBrain NeoplasmsCell ProliferationCells, CulturedDisease ProgressionE2F7 Transcription FactorEnhancer of Zeste Homolog 2 ProteinGene Expression Regulation, NeoplasticGlioblastomaHEK293 CellsHumansMaleMiceMice, NudeNeoplasm MetastasisProto-Oncogene Proteins c-aktE2F7 protein, humanE2F7 Transcription FactorEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanMTOR protein, humanProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID32814835
PMCPMC7591888
OpenAlexW3055581418

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.