Evidence map›Paper›PMID 30564960›Full record

Trial reportMolecular and cellular biochemistry2019

IL-17A/IL-17RA promotes invasion and activates MMP-2 and MMP-9 expression via p38 MAPK signaling pathway in non-small cell lung cancer.

Zhenhua Wu, Dan He, Shuyuan Zhao, Hongjiang Wang

Abstract readClinical Trial
PubMed Publisher
In one paragraph

Trial report in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
2.3field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 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

4 authors at 1 institution in 1 country.

Zhenhua WuDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No. 789 East Suzhou Road, Ürümqi, 830000, Xinjiang Uygur Autonomous Region, People's Republic of China.
Dan HeDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No. 789 East Suzhou Road, Ürümqi, 830000, Xinjiang Uygur Autonomous Region, People's Republic of China.
Shuyuan ZhaoDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No. 789 East Suzhou Road, Ürümqi, 830000, Xinjiang Uygur Autonomous Region, People's Republic of China.
Hongjiang WangDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No. 789 East Suzhou Road, Ürümqi, 830000, Xinjiang Uygur Autonomous Region, People's Republic of China. whj71210@sina.com.
Xinjiang Medical University · CN

Funding

the National Natural Science Foundation of China No. 81460354
6 · The paper itself

Abstract

The present study is to investigate the effect and mechanism of action of interleukin (IL)-17A and its receptor IL-17RA on non-small cell lung cancer (NSCLC). A total of 139 NSCLC patients were included in the study. NSCLC tissues and tumor-adjacent tissues were collected from the patients. Human NSCLC cell lines H157, H1975, and A549 were used for in vitro studies. MTT assay was performed to determine cell proliferation. Wound healing assay was used to determine cell motility. Transwell assay was carried out to detect migration and invasion. Quantitative real-time polymerase chain reaction was conducted to measure mRNA expression, while Western blotting was used for determine protein expression. Immunohistochemistry was employed to evaluate IL-17RA expression in 139 primary human NSCLC tissues. Levels of IL-17RA in NSCLC tissues were higher than tumor-adjacent normal tissues, and associated with clinical outcomes. Kaplan-Meier survival analysis indicated that NSCLC patients with positive IL-17RA expression had a poor survival. In addition, IL-17A/IL-17RA affected NSCLC cell migration and invasion in vitro. Treatment with IL-17A/IL-17RA increased the expression of MMP-2 and MMP-9 in NSCLC cells. Furthermore, phosphorylation of p38 was enhanced in IL-17RA-overexpressing NSCLC cells. P38 MAPK-specific inhibitor SB203580 suppressed the migration and invasion of NSCLC cells. MMP-2 and MMP-9 were downstream effectors of IL-17RA and p38 signaling pathways. The present study demonstrates that P38 MAPK activity is crucial for IL-17A/IL-17RA to promote NSCLC metastasis. In addition, IL-17A/IL-17RA signaling may be a novel and promising cancer therapeutic target for the treatment of NSCLC.

Indexed as

MAP Kinase Signaling SystemAdultAgedCarcinoma, Non-Small-Cell LungFemaleHumansInterleukin-17Lung NeoplasmsMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9Middle AgedNeoplasm InvasivenessNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesReceptors, Interleukin-17IL17A protein, humanIL17RA protein, humanInterleukin-17Matrix Metalloproteinase 2Matrix Metalloproteinase 9MMP2 protein, humanMMP9 protein, humanNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesReceptors, Interleukin-17IL-17A/IL-17RAMMP-2MMP-9Non-small cell lung cancerP38 MAPK signaling pathway

Identifiers

PMID30564960
OpenAlexW2904970316

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.