Evidence map›Paper›PMID 27286259›Full record

ArticleOncotarget2016

TLR4/ROS/miRNA-21 pathway underlies lipopolysaccharide instructed primary tumor outgrowth in lung cancer patients.

Xianqi Zhang, Chunhong Wang, Shan Shan, Xiyu Liu, Zhongmin Jiang, Tao Ren

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  16. The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress.International journal of molecular sciences · 2020
    Review
  17. MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases.International journal of molecular sciences · 2020
    Review
  18. Article
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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

6 authors at 4 institutions in 1 country.

Xianqi ZhangDepartment of Thoracic Surgery, Qianfoshan Hospital, Shandong University, Shandong 250014, China.
Chunhong WangDepartment of Respiratory Medicine, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Shan ShanDepartment of Respiratory Medicine, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Xiyu LiuDepartment of Thoracic Surgery, Affiliated Hospital of Guilin Medical University, Guilin 541001, China.
Zhongmin JiangDepartment of Thoracic Surgery, Qianfoshan Hospital, Shandong University, Shandong 250014, China.
Tao RenDepartment of Respiratory Medicine, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Shanghai East Hospital · CNGuilin Medical University · CNShandong Provincial QianFoShan Hospital · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of Toll-like receptor 4 (TLR4) signaling in human lung cancer with lipopolysaccharide (LPS) enhances tumor progression. However, whether primary human lung cancer outgrowth could respond to LPS and underlying mechanisms are unclear. Here we determined that TLR4 activation with LPS promoted outgrowth of primary human lung cancer cells in vitro and in vivo. Mechanistically, LPS stimulation increased expression levels of microRNA-21 (miR-21) in primary human lung cancer cells. Inhibition of miR-21 blocked the enhanced lung cancer growth induced by LPS in vitro and in vivo. Up-regulation of miR-21 promoted outgrowth of primary human lung cancer. Down-regulation of miR-21 limited primary human lung cancer outgrowth. Further, TLR4 activation in primary human lung cancer cells increased their ROS levels. Scavenge of ROS abrogated the up-regulation of miR-21 in primary human lung cancer cells and attenuated LPS-induced outgrowth. For in vivo relevance, expression of TLR4 was correlated with miR-21 expression and ROS production in freshly isolated, untreated primary human lung cancer cells. These findings demonstrate an essential role of TLR4/ROS/miR-21 pathway in LPS-induced outgrowth of primary human lung cancer. Our study connected a framework of innate signaling, oxidative stress and microRNA in tumor immunity and provided clues for developing new therapeutics for lung cancer.

Indexed as

Gene Expression Regulation, NeoplasticAgedAnimalsFemaleHumansLipopolysaccharidesLungLung NeoplasmsMaleMiceMice, Inbred BALB CMicroRNAsMiddle AgedNeoplasm TransplantationReactive Oxygen SpeciesSignal TransductionLipopolysaccharidesMicroRNAsMIRN21 microRNA, humanReactive Oxygen SpeciesTLR4 protein, humanToll-Like Receptor 4LPSlung cancermiR-21ROSTLR4

Identifiers

PMID27286259
PMCPMC5173125
OpenAlexW2409719348

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.