Evidence map›Paper›PMID 27166634›Full record

ArticleLung2016

ANGPTL4 Correlates with NSCLC Progression and Regulates Epithelial-Mesenchymal Transition via ERK Pathway.

Xiaoming Zhu, Xiaobin Guo, Sen Wu, Li Wei

Abstract read
PubMed Publisher
In one paragraph

Article in Lung, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  15. ANGPTL4 Regulates PsoriasisFrontiers in pharmacology · 2022
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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 2 institutions in 1 country.

Xiaoming ZhuDepartment of Thoracic Surgery, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Zhengzhou, 450000, Henan, China.
Xiaobin GuoDepartment of Respiratory Disease, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Zhengzhou, 450000, Henan, China.
Sen WuDepartment of Thoracic Surgery, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Zhengzhou, 450000, Henan, China.
Li WeiDepartment of Thoracic Surgery, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Zhengzhou, 450000, Henan, China. thoracicweili@163.com.
Henan Provincial People's Hospital · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose Lung cancer remains the leading cause of cancer deaths with intricate mechanisms. In the present study, we evaluated the clinical significance and biological role of ANGPTL4 in non-small cell lung cancer (NSCLC), the most common lung cancer subtype. Methods Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used for examining the mRNA level of ANGPTL4 in NSCLC tissues and adjacent non-tumor tissues, NSCLC cell lines, and the immortalized human bronchial epithelial cell line HBE, respectively. A tissue microarray was used for analyzing the relationship between ANGPTL4 expression and the clinicopathological parameters of NSCLC patients. Commercial lentivirus expressing shRNAs was used for silencing ANGPTL4. Cell Counting Kit-8 (CCK-8) was employed for evaluating the cell proliferation ability and transwell with or without matrigel was used for cell migration and invasion assay. Results As the result, ANGPTL4 was over-expressed in NSCLC tissues compared with benign lung tissues. Silencing ANGPTL4 expression strongly inhibited the proliferation, migration, and invasion of A549 and H520 cells, which was in accordance with the increase of epithelial marker E-cadherin and decrease of mesenchymal marker vimentin. By screening the ERK, AKT, EGFR, and STAT3 pathways, we found that cell growth, migration, and invasion arrest induced by loss of ANGPTL4 expression was partially attributable to down-regulation of ERK signaling. Conclusion These results suggested that ANGPTL4 was essential for proliferation and metastasis of lung cancer cells and might serve as a novel target for the treatment of lung cancer.

Indexed as

A549 CellsAngiopoietin-Like Protein 4CadherinsCarcinoma, Non-Small-Cell LungCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene ExpressionGene SilencingHumansLungLung NeoplasmsMaleMAP Kinase Signaling SystemAngiopoietin-Like Protein 4ANGPTL4 protein, humanCadherinsRNA, MessengerVimentinANGPTL4Epithelial-mesenchymal transitionERKNSCLC

Identifiers

PMID27166634
OpenAlexW2377002235

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.