Evidence map›Paper›PMID 33829382›Full record

ArticleEnvironmental science and pollution research international2021

LncRNA NEAT1 contributes to the acquisition of a tumor like-phenotype induced by PM 2.5 in lung bronchial epithelial cells via HIF-1α activation.

Pan Jiang, Shengyu Hao, Liang Xie, Guiling Xiang, Weiping Hu, Qinhan Wu, Zilong Liu, Shanqun Li

Abstract read
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In one paragraph

Article in Environmental science and pollution research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

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  6. Particulate matter-induced epigenetic modifications and lung complications.European respiratory review : an official journal of the European Respiratory Society · 2024
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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 4 institutions in 1 country.

Pan Jiang *Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Shengyu Hao *Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Liang XieDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Guiling XiangDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Weiping HuDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Qinhan WuDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Zilong LiuDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Shanqun LiDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China. shanqun@zs-hospital.sh.cn.
Sun Yat-sen University · CNFudan University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNZhongshan Hospital · CN

Funding

The National Key Research and Development Program of China No. 2018YFC1313600
6 · The paper itself

Abstract

The hazards of particulate matter (PM2.5) on human respiratory health have been previously reported. However, the molecular mechanisms underlying PM2.5-induced lung carcinogenesis have rarely been studied. In the present study, we explored the effects of PM2.5 on the epithelial-mesenchymal transition (EMT) and acquisition of cancer stem cell (CSC)-like properties in lung bronchial epithelial cells. We found that exposure of PM2.5 enhanced lung bronchial epithelial cell proliferation and EMT. In addition, the expression level of CSC-like biomarkers, CD133 and CD44, was significantly elevated by PM2.5 in vitro. Nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported to participate in lung cancer. Loss of NEAT1 represses the malignant transformation of BEAS-2B and HBE cells induced by PM2.5. NEAT1 interacts with microRNA (miR)-582-5p, and miR-582-5p reverses the pro-tumor effects of NEAT1 overexpression. Hypoxia-inducible factor (HIF)-1α is an important transcription factor in the pathological responses to hypoxia. HIF-1α was a predicted target for miR-582-5p, and a direct correlation between them was identified. Inhibitors of miR-582-5p rescued HIF-1α expression, which was attenuated by a lack of NEAT1. In conclusion, PM2.5 increased NEAT1 expression, which, by binding with miR-582-5p, released HIF-1α and promoted EMT and the acquisition of CSC-like characteristics.

Indexed as

Lung NeoplasmsRNA, Long NoncodingCell Line, TumorCell MovementEpithelial CellsGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitLungMicroRNAsParticulate MatterPhenotypeHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN582 microRNA, humanNEAT1 long non-coding RNA, humanParticulate MatterRNA, Long NoncodingCancer stem cellsHIF-1αLung cancermiR-582-5pNEAT1Particulate matter

Identifiers

PMID33829382
OpenAlexW3146105830

What OpenQuestion holds

Textmetadata
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.