Evidence map›Paper›PMID 32440144›Full record

ArticleOncoTargets and therapy2020

Alpha-1 Antitrypsin Induces Epithelial-to-Mesenchymal Transition, Endothelial-to-Mesenchymal Transition, and Drug Resistance in Lung Cancer Cells.

Dong-Ming Wu, Teng Liu, Shi-Hua Deng, Rong Han, Ting Zhang, Jing Li, Ying Xu

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  8. Serum α1-AT Levels andDiseases (Basel, Switzerland) · 2024
    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

7 authors at 1 institution in 1 country.

Dong-Ming Wu *Clinical Laboratory, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan 610041, People's Republic of China.
Teng Liu *Clinical Laboratory, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan 610041, People's Republic of China.ORCID 0000-0001-8300-8654
Shi-Hua DengClinical Laboratory, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan 610041, People's Republic of China.
Rong HanClinical Laboratory, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan 610041, People's Republic of China.
Ting ZhangClinical Laboratory, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan 610041, People's Republic of China.
Jing LiClinical Laboratory, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan 610041, People's Republic of China.
Ying XuClinical Laboratory, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan 610041, People's Republic of China.ORCID 0000-0001-9570-8666
First Affiliated Hospital of Chengdu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAlpha-1 antitrypsin (A1AT) is a secreted protein that plays an important role in various diseases. However, the role of A1AT in non-small cell lung cancer is obscure. MATERIALS AND

methodsA1AT expression in non-small cell lung cancer was analyzed using quantitative reverse transcription PCR, Western blotting (WB), immunohistochemistry (IHC), and ELISA. WB and IF were used to analyze markers of epithelial-to-mesenchymal transition (EMT), EndoMT, and cancer stem cell (CSC). Transwell and cell wound healing assays were used to analyze migration and invasion abilities. Colony formation and CCK-8 assays were used to analyze cell proliferation following cisplatin treatment.

resultsA1AT expression was higher in lung cancer samples than in normal tissues and the increased expression was correlated with poor overall survival of patients. In vitro experiments showed that A1AT overexpressed by plasmid transfection significantly promoted migration, invasion, EMT, EndoMT, stemness, and colony formation in lung cancer cell lines, as opposed to A1AT downregulation by siRNA transfection, which significantly inhibited all these variables.

conclusionA1AT is a novel therapeutic target and might be associated with tumor metastasis in lung carcinoma.

Indexed as

alpha-1 antitrypsincisplatin resistanceendothelial-to-mesenchymal transitionepithelial-to-mesenchymal transitionnon-small cell lung cancer

Identifiers

PMID32440144
PMCPMC7210034
OpenAlexW3023539659

What OpenQuestion holds

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LicenceCC BY-NC
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.