Evidence map›Paper›PMID 31275431›Full record

ArticleTherapeutic advances in medical oncology2019

EGFR-AS1/HIF2A regulates the expression of FOXP3 to impact the cancer stemness of smoking-related non-small cell lung cancer.

Haolong Qi, Shanshan Wang, Juekun Wu, Shucai Yang, Steven Gray, Calvin S H Ng, Jing Du, Malcolm J Underwood, Ming-Yue Li, George G Chen

Open access · goldAbstract read
In one paragraph

Article in Therapeutic advances in medical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 35% 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

17 citing papers in PubMed, 21 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

10 authors at 5 institutions in 3 countries.

Haolong QiDepartment of Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China.
Shanshan WangDepartment of Otorhinolaryngology, Head and Neck Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China.
Juekun WuDepartment of Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Shucai YangDepartment of Clinical Laboratory, Pingshan District People's Hospital of Shenzhen, Shenzhen, China.
Steven GrayThoracic Oncology Research Group, Trinity Centre for Health Sciences, St James's Hospital, Dublin, Ireland.
Calvin S H NgDepartment of Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China.
Jing DuPeking University Shenzhen Hospital, Shenzhen, China.
Malcolm J UnderwoodDepartment of Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China.
Ming-Yue LiDepartment of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
George G ChenDepartment of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.ORCID https://orcid.org/0000-0001-7276-3830
Chinese University of Hong Kong · HKPeking University Shenzhen Hospital · CNShenzhen Sixth People's Hospital · CNSun Yat-sen University · CNTrinity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEarly data showed that FOXP3 could induce epithelial-mesenchymal transition by stimulating the Wnt/β-catenin signaling pathway in non-small cell lung cancer (NSCLC). However, how the expression of FOXP3 is regulated in NSCLC remains unknown. We thus explored the impacts of the long noncoding RNA EGFR antisense RNA 1 (EGFR-AS1) and hypoxia-inducible factor-2A (HIF2A) on FOXP3 expression and the cancer stemness of NSCLC.

methodsLung tissues samples from 87 patients with NSCLC and two NSCLC cell lines were used in this study. The regulation of FOXP3 and lung cancer cell stemness by EGFR-AS1 and HIF2A was determined at molecular levels in NSCLC tissue samples and cultured cells in the presence/absence of the smoking carcinogen, 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (also known as nicotine-derived nitrosamine ketone). The results were confirmed in tumor xenograft models.

resultsWe found that NNK decreased the expression of EGFR-AS1 in the long term, but increased the expression of HIF2A and FOXP3 to stimulate lung cancer cell stemness. EGFR-AS1 significantly inhibited FOXP3 expression and NSCLC cell stemness, whereas HIF2A obviously promoted both. The enhancement of lung cancer stemness by FOXP3 was, at least partially,

conclusionsFOXP3, the expression of which is under the fine control of EGFR-AS1, is a critical molecule that promotes NSCLC cancer cell stemness through stimulating the Notch1 pathway.

Indexed as

cancer cell stemnessEGFR antisense RNA 1FOXP3hypoxia-inducible factor-2 alphanon-small cell lung cancer

Identifiers

PMID31275431
PMCPMC6598324
OpenAlexW2949316736

What OpenQuestion holds

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LicenceCC BY-NC
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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.