Evidence map›Paper›PMID 32268297›Full record

ArticleAging2020

Inhibiting Forkhead box K1 induces autophagy to reverse epithelial-mesenchymal transition and metastasis in gastric cancer by regulating Myc-associated zinc finger protein in an acidic microenvironment.

Yixuan Wang, Libin Sun, Wensheng Qiu, Weiwei Qi, Yaoyue Qi, Zhao Liu, Shihai Liu, Jing Lv

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 29 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

8 authors at 2 institutions in 1 country.

Yixuan WangDepartment of Oncology, Affiliated Hospital of Qingdao University, Qingdao 266071, Shandong, China.
Libin SunDepartment of Oncology, Affiliated Hospital of Qingdao University, Qingdao 266071, Shandong, China.
Wensheng QiuDepartment of Oncology, Affiliated Hospital of Qingdao University, Qingdao 266071, Shandong, China.
Weiwei QiDepartment of Oncology, Affiliated Hospital of Qingdao University, Qingdao 266071, Shandong, China.
Yaoyue QiDepartment of Oncology, Affiliated Hospital of Qingdao University, Qingdao 266071, Shandong, China.
Zhao LiuDepartment of Oncology, Affiliated Hospital of Qingdao University, Qingdao 266071, Shandong, China.
Shihai LiuCentral Laboratory, Affiliated Hospital of Qingdao University, Qingdao 266071, Shandong, China.
Jing LvDepartment of Oncology, Affiliated Hospital of Qingdao University, Qingdao 266071, Shandong, China.
Qingdao University · CNAffiliated Hospital of Qingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundForkhead box K1 (FOXK1) is a transcription factor belonging to the Forkhead box (FOX) family and is closely related to the development of various cancers, but the functional mechanism through which FOXK1 regulates autophagy and epithelial-mesenchymal transition (EMT) in the acidic microenvironment of gastric cancer (GC) remains unclear.

resultsOur results indicated that the inhibition of FOXK1 induced autophagy and thus exerted antimetastatic effects in an acidic microenvironment. The dual inhibition of mammalian target of rapamycin (mTOR) and FOXK1 enhanced autophagy and reversed EMT of acidic GC cells. In addition, FOXK1 activated transcription in conjunction with the MAZ promoter.

conclusionTogether, our results suggest that FOXK1 can be used as an independent prognostic indicator for GC patients. We also revealed a new strategy involving the cotargeting of FOXK1 and autophagy to reverse the effects of EMT. MAZ is involved in the development and progression of GC as a downstream target of FOXK1.

methodsHere, the cellular responses to the inhibition of FOXK1 in GC were studied in vivo and in vitro through wound healing assays, transwell assays, Western blotting, laser confocal microscopy and transmission electron microscopy. The molecular mechanisms of FOXK1 and Myc-associated zinc finger protein (MAZ) were studied via chromatin immunoprecipitation sequencing (ChIP-seq), bioinformatics, Western blotting, and quantitative real-time PCR (q-PCR).

Indexed as

Stomach NeoplasmsTumor MicroenvironmentAnimalsAutophagyCell Line, TumorDNA-Binding ProteinsDown-RegulationEpithelial-Mesenchymal TransitionForkhead Transcription FactorsGene SilencingHumansHydrogen-Ion ConcentrationMiceNeoplasm InvasivenessNeoplasm MetastasisProto-Oncogene Proteins c-mycc-MYC-associated zinc finger proteinDNA-Binding ProteinsForkhead Transcription FactorsFOXK1 protein, humanMTOR protein, humanProto-Oncogene Proteins c-mycTOR Serine-Threonine KinasesTranscription FactorsautophagyEMTFOXK1gastric cancerMAZ

Identifiers

PMID32268297
PMCPMC7185099
OpenAlexW3014524014

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.