Evidence map›Paper›PMID 37449511›Full record

ArticleInternational journal of molecular medicine2023

E74‑like ETS transcription factor 5 facilitates cell proliferation through regulating the expression of adenomatous polyposis coli 2 in non‑small cell lung cancer.

Jing Wen, Genggeng Qin, Zhaojing Jiang, Zixun Lin, Ruixin Zhou, Hui Dai, Zhanfa Xu, Weiguo Chen, Qiancheng Song

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 4 institutions in 1 country.

Jing Wen *Department of Radiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Genggeng Qin *Department of Radiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Zhaojing Jiang *Department of Radiation Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
Zixun LinDepartment of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Ruixin ZhouDepartment of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Hui DaiHospital Office, Ganzhou Hospital‑Nanfang Hospital, Southern Medical University, Ganzhou, Jiangxi 341000, P.R. China.
Zhanfa XuDepartment of Radiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Weiguo ChenDepartment of Radiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Qiancheng SongDepartment of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Nanfang Hospital · CNSouthern Medical University · CNGanzhou People's Hospital · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

E74‑like ETS transcription factor 5 (ELF5) is known to regulate the specification and differentiation of epithelial cells in the embryonic lung. However, the pathological function of ELF5 in lung cancer has yet to be fully elucidated. In the present study, the expression of ELF5 was found to be significantly higher in lung adenocarcinoma compared with that in corresponding adjacent normal tissues. Subsequently, cell and animal experiments were performed to investigate the role of ELF5 in lung adenocarcinoma cells. The results indicated that the overexpression of ELF5 increased the proliferation of lung adenocarcinoma cells, whereas, by contrast, a reduction in the expression of ELF5 led to a decrease in their proliferation. Mechanistically, the hypothesis is advanced that ELF5 can promote lung cancer cell proliferation through inhibiting adenomatous polyposis coli 2 and increasing the expression of cyclin D1, which is a critical downstream target of the Wnt pathway. Taken together, these findings support the notion that ELF5 exerts an essential role in the proliferation of lung adenocarcinoma cells and may be a therapeutic target for the treatment of lung adenocarcinoma.

Indexed as

Adenocarcinoma of LungAdenomatous Polyposis ColiCarcinoma, Non-Small-Cell LungLung NeoplasmsAnimalsCell ProliferationDNA-Binding ProteinsProto-Oncogene Proteins c-etsTranscription FactorsDNA-Binding ProteinsProto-Oncogene Proteins c-etsTranscription FactorsELF5lung adenocarcinomaproliferation

Identifiers

PMID37449511
PMCPMC10555483
OpenAlexW4383955300

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.