Evidence map›Paper›PMID 30854106›Full record

ArticleJournal of Cancer2019

Tumor-associated inflammatory microenvironment in non-small cell lung cancer: correlation with FGFR1 and TLR4 expression via PI3K/Akt pathway.

Ruhui Zhang, Yongquan Dong, Mingjiao Sun, Yina Wang, Changqing Cai, Yun Zeng, Yueguang Wu, Qiong Zhao

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2019. 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
1.5field-weighted citation impact, top 18% 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, 26 citations in OpenAlex.

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  12. Targeting Toll-like receptor 4 with CLI-095 (TAK-242) enhances the antimetastatic effect of the estrogen receptor antagonist fulvestrant on non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
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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.

Ruhui ZhangDepartment of Respiratory Diseases, The First Affiliated Hospital of Zhejiang University, Hangzhou 310003, Zhejiang, People's Republic of China.
Yongquan DongDepartment of Respiratory Diseases, Ningbo No.2 hospital, Ningbo 315100, People's Republic of China.
Mingjiao SunDepartment of Thoracic Oncology, Hangzhou Cancer Hospital, Hangzhou 310002, Zhejiang, People's Republic of China.
Yina WangDepartment of Medical Oncology, The First Affiliated Hospital of Zhejiang University, Hangzhou 310003, Zhejiang, People's Republic of China.
Changqing CaiDepartment of surgery, Xinsheng Group, Hangzhou 310003, Zhejiang, People's Republic of China.
Yun ZengDepartment of Thoracic Oncology, Hangzhou Cancer Hospital, Hangzhou 310002, Zhejiang, People's Republic of China.
Yueguang WuDepartment of Thoracic Oncology, Hangzhou Cancer Hospital, Hangzhou 310002, Zhejiang, People's Republic of China.
Qiong ZhaoDepartment of Thoracic Oncology, Hangzhou Cancer Hospital, Hangzhou 310002, Zhejiang, People's Republic of China.
Zhejiang Cancer Hospital · CNHangzhou First People's Hospital · CNNingbo No. 2 Hospital · CNZhejiang Lab · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor-associated inflammatory microenvironment plays a pivotal role in human non-small cell lung cancer (NSCLC) development. FGFR1 and TLR4 involve in the regulation of inflammatory microenvironment of NSCLC.However, the relationship between the FGFR1 and TLR4 signaling and the mechanisms that involved in tumor-associated microenvironment are still unclear. We investigated the expression of FGFR1 and TLR4 in cancerous tissues and noncancerous lung tissues from 60 primary NSCLC patients using immunohistochemical staining. Three cell lines (A549, PC-9 and SK-MES-1) were used for in vitro studies. We demonstrated that the expression of FGFR1 and TLR4 was significantly correlated (r=0.504, p<0.05) in NSCLC tissues. We revealed that activation of FGFR1 and TLR4 pathways by specific signaling agonist increased Akt phosphorylation. Further results showed that FGFR1 and TLR4 regulated cell proliferation and migration and promoted the production of proinflammatory or immunosuppressive cytokines TNF-α and IL-6. Meanwhile, the PI3K inhibitor LY294002 rescued these changes. Taken together, our results indicate that the FGFR1 expression level is positively correlated with TLR4 expression level in human NSCLC tissues. The activation of FGFR1 and TLR4 in cancer cells contributes to inflammatory microenvironment via PI3K/Akt signaling and may make a significant contribution to the progression of human NSCLC.

Indexed as

FGFR1NSCLCphosphatidylinositol 3-kinase (PI3K)/AktTLR4tumor-associated inflammatory

Identifiers

PMID30854106
PMCPMC6400805
OpenAlexW2913869045

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.