Evidence map›Paper›PMID 33713575›Full record

ArticleFEBS open bio2021

Interleukin-36α suppresses growth of non-small cell lung cancer in vitro by reducing angiogenesis.

Xiaoxiao Xie, Haoyue Hu, Jun He, Yanyang Liu, Fengzhu Guo, Feng Luo, Ming Jiang, Li Wang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 51% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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.

Xiaoxiao XieLung Cancer Center, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Haoyue HuLung Cancer Center, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Jun HeLung Cancer Center, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.ORCID 0000-0001-5842-5878
Yanyang LiuLung Cancer Center, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Fengzhu GuoLung Cancer Center, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Feng LuoLung Cancer Center, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Ming JiangCancer Center, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Li WangLung Cancer Center, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Sichuan University · CNUniversity of Electronic Science and Technology of China · CN

Funding

Health Commission of Mianyang City 201706National Natural Science Foundation of China NO.81802512Science and Technology Department of Sichuan Province 2017SZ0103
6 · The paper itself

Abstract

Interleukin (IL)-36α, a newly recognized IL-1 family member, has been previously reported to play a pivotal role in autoimmunity diseases and acute inflammatory reactions. Recently, several studies have indicated that IL-36α has potential anticancer effects against certain types of cancer. However, the expression pattern and functional role of IL-36α in non-small cell lung cancer (NSCLC) have not been elucidated. Here, we report that the mRNA and protein levels of IL-36α are significantly reduced in NSCLC tissues. Low levels of intratumoral IL-36α are correlated with higher tumor status, advanced TNM stage, increased vascular invasion and shorter overall survival (OS). Intratumoral IL-36α expression is an independent prognostic factor for OS (hazard ratio = 3.081; P = 0.012) in patients with NSCLC. Overexpression of IL-36α in lung cancer cells did not disturb cell proliferation, apoptosis or cell-cycle distribution in vitro, but markedly inhibited tumor growth in vivo. Mechanistically, IL-36α reduced the expression and secretion of vascular endothelial growth factor A through inhibiting hypoxia-inducible factor 1α expression. Finally, decreased IL-36α expression was associated with high microvessel density and vascular endothelial growth factor A in patients with NSCLC. Together, our findings suggest that IL-36α expression is a valuable marker indicating poor prognosis in patients with NSCLC.

Indexed as

AdultAgedAged, 80 and overCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationChinaFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansInterleukin-1InterleukinsLung NeoplasmsMaleMiddle AgedIL36A protein, humanInterleukin-1InterleukinsRNA, Messengerangiogenesisinterleukin-36αnon-small cell lung cancerVEGFA

Identifiers

PMID33713575
PMCPMC8091581
OpenAlexW3136506230

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.