Evidence map›Paper›PMID 33980247›Full record

ArticleCell communication and signaling : CCS2021

ATF5 and HIF1α cooperatively activate HIF1 signaling pathway in esophageal cancer.

Feng He, Hang Xiao, Yixin Cai, Ni Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 18 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

4 authors at 1 institution in 1 country.

Feng HeDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology, Wuhan, 430030, China.ORCID 0000-0002-7034-4285
Hang XiaoDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology, Wuhan, 430030, China.
Yixin CaiDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology, Wuhan, 430030, China.
Ni ZhangDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology, Wuhan, 430030, China. zhangnidoc@vip.163.com.
Tongji Hospital · CN

Funding

Double first class construction project of Tongji Medical College of Huazhong University of science and technology--Research clinician funding scheme 3011540027Double first class construction project of Tongji Medical College of Huazhong University of science and technology--Research clinician funding scheme 5001540077Natural Science Foundation of Hubei Province 2016CFB550
6 · The paper itself

Abstract

backgroundEsophageal cancer (ESCA) is one of the most common cancers worldwide and has a very poor prognosis. Hypoxia-inducible factor 1 (HIF1) signaling pathway plays a critical role in tumorigenesis and is therefore considered a potential therapeutic target in the treatment of many cancers. Activating transcription factor 5 (ATF5) facilitates the expression of various genes and has been extensively studied for its potential role in cancer treatment.

methodsThe expression level of ATF5 in clinic sample was detected by quantitative real time PCR and immunohistochemistry. ATF5 biological function was investigated by western blot, cell cycle analysis, cell viability assay, luciferase reporter assays, colony formation assay, transwell assay, wound healing assay, tube formation assay, and ELISA assay. CHIP and Re-CHIP assay, GST-pulldown, and RNA-sequencing were used to study the cross-talks between ATF5 and HIF1 complex. Mouse xenograft study was utilized to study the correlation of ATF5 and tumor growth in vivo. Student's t-test or Chi-square test was used for statistical analysis.

resultsHere, we first found ATF5 was dramatically upregulated in ESCA cancer and related with poor survival time. Next, we found that the expression level of ATF5 had a positive relationship with the proliferation, migration, and invasion ability of ESCA cells. Besides, we innovatively found that ATF5 functions as a novel coactivator in HIF1 transcription complex by binding to HIF1α. Further, we demonstrated that silencing ATF5 phenocopies HIF1α knockdown in tumorigenic properties in vitro and inhibited ESCA tumor angiogenesis and proliferation in vivo.

conclusionHerein, we found ATF5 as a novel component of the HIF1 transcription complex. The findings of the present study may provide new insights into the development of a novel and more efficient therapeutic strategy against ESCA. Video abstract.

Indexed as

Signal TransductionActivating Transcription FactorsAnimalsCarcinogenesisCell Line, TumorCell MovementCell ProliferationEsophageal NeoplasmsGene Expression Regulation, NeoplasticGene SilencingHumansHuman Umbilical Vein Endothelial CellsHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMice, Inbred BALB CActivating Transcription FactorsATF5 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitATF5Esophageal cancerHIF1

Identifiers

PMID33980247
PMCPMC8117505
OpenAlexW3162542659

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Registered trials

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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.