Evidence map›Paper›PMID 28195146›Full record

ArticleScientific reports2017

The inhibition of lung cancer cell migration by AhR-regulated autophagy.

Chi-Hao Tsai, Ching-Hao Li, Yu-Wen Cheng, Chen-Chen Lee, Po-Lin Liao, Cheng-Hui Lin, Shih-Hsuan Huang, Jaw-Jou Kang

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

27 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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.

Chi-Hao TsaiInstitute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ching-Hao LiDepartment of Physiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Yu-Wen ChengSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei, Taiwan.
Chen-Chen LeeDepartment of Microbiology and Immunology, School of Medicine, China Medical University, Taichung, Taiwan.
Po-Lin LiaoInstitute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Cheng-Hui LinSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei, Taiwan.
Shih-Hsuan HuangSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei, Taiwan.
Jaw-Jou KangInstitute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that is highly expressed in multiple organs and tissues. Whereas AhR mediates the metabolism of xenobiotic and endogenous compounds, its novel function in cancer epithelial-mesenchymal transition (EMT) remains controversial. Autophagy also participates in tumour progression through its functions in cell homeostasis and facilitates adaptation to EMT progression. In the present study, we found that AhR-regulated autophagy positively modulates EMT in non-small cell lung cancer cells. The motility of A549, H1299, and CL1-5 cells were correlated with different AhR expression levels. Invasive potential and cell morphology also changed when AhR protein expression was altered. Moreover, AhR levels exerted a contrasting effect on autophagy potential. Autophagy was higher in CL1-5 and H1299 cells with lower AhR levels than in A549 cells. Both AhR overexpression and autophagy inhibition decreased CL1-5 metastasis in vivo. Furthermore, AhR promoted BNIP3 ubiquitination for proteasomal degradation. AhR silencing in A549 cells also reduced BNIP3 ubiquitination. Taken together, these results provide a novel insight into the cross-linking between AhR and autophagy, we addressed the mechanistic BNIP3 modulation by endogenous AhR, which affect cancer cell EMT progression.

Indexed as

AutophagyEpithelial-Mesenchymal TransitionAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementHumansLung NeoplasmsMembrane ProteinsMiceMice, Inbred ICRMitochondrial ProteinsReceptors, Aryl HydrocarbonUbiquitinationBNip3 protein, mouseMembrane ProteinsMitochondrial ProteinsReceptors, Aryl Hydrocarbon

Identifiers

PMID28195146
PMCPMC5307309

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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.