Evidence map›Paper›PMID 29115924›Full record

ArticleBMC cancer2017

Transcription factor E2F1 promotes EMT by regulating ZEB2 in small cell lung cancer.

Tingting Wang, Xufang Chen, Weiwei Qiao, Lijun Kong, Daqing Sun, Zunling Li

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.8field-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

49 citing papers in PubMed, 102 citations in OpenAlex.

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  14. Post-Translational Modification of ZEB Family Members in Cancer Progression.International journal of molecular sciences · 2022
    Review
  15. 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 3 institutions in 1 country.

Tingting WangDepartment of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, 264003, China.
Xufang ChenOncology Department, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, 264199, China.
Weiwei QiaoDepartment of Diagnostics, Binzhou Medical University, Yantai, 264003, China.
Lijun KongDepartment of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, 264003, China.
Daqing SunTianjin Medical University General Hospital, Tianjin, 300052, China. sundaqingchris@126.com.
Zunling LiDepartment of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, 264003, China. lizunling@bzmc.edu.cn.
Binzhou University · CNBinzhou Medical University · CNTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpithelial-mesenchymal transition (EMT) is an early event in tumour invasion and metastasis, and widespread and distant metastasis at early stages is the typical biological behaviour in small cell lung cancer (SCLC). Our previous reports showed that high expression of the transcription factor E2F1 was involved in the invasion and metastasis of SCLC, but the role of E2F1 in the process of EMT in SCLC is unknown.

methodsImmunohistochemistry was performed to evaluate the expressions of EMT related markers. Immunofluorescence was used to detect the expressions of cytoskeletal proteins and EMT related markers when E2F1 was silenced in SCLC cell lines. Adenovirus containing shRNA against E2F1 was used to knock down the E2F1 expression, and the dual luciferase reporter system was employed to clarify the regulatory relationship between E2F1 and ZEB2.

resultsIn this study, we observed the remodelling of cytoskeletal proteins when E2F1 was silenced in SCLC cell lines, indicating that E2F1 was involved in the EMT in SCLC. Depletion of E2F1 promoted the expression of epithelial markers (CDH1 and CTNNB1) and inhibited the expression of mesenchymal markers (VIM and CDH2) in SCLC cell lines, verifying that E2F1 promotes EMT occurrence. Next, the mechanism by which E2F1 promoted EMT was explored. Among the CDH1 related inhibitory transcriptional regulators ZEB1, ZEB2, SNAI1 and SNAI2, the expression of ZEB2 was the highest in SCLC tissue samples and was highly consistent with E2F1 expression. ChIP-seq data and dual luciferase reporter system analysis confirmed that E2F1 could regulate ZEB2 gene expression.

conclusionOur data supports that E2F1 promotes EMT by regulating ZEB2 gene expression in SCLC.

Indexed as

Epithelial-Mesenchymal TransitionCell Line, TumorCell MovementCell ProliferationE2F1 Transcription FactorFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMalePromoter Regions, GeneticSmall Cell Lung CarcinomaUp-RegulationZinc Finger E-box Binding Homeobox 2E2F1 protein, humanE2F1 Transcription FactorZEB2 protein, humanZinc Finger E-box Binding Homeobox 2E2F1Epithelial-mesenchymal transitionSmall cell lung cancerZEB2

Identifiers

PMID29115924
PMCPMC5678576
OpenAlexW2767436434

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.