Evidence map›Paper›PMID 30816464›Full record

ArticleMolecular medicine reports2019

PADI4‑mediated epithelial‑mesenchymal transition in lung cancer cells.

Meiyan Liu, Yang Qu, Xue Teng, Ying Xing, Dandan Li, Chunhong Li, Li Cai

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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  15. Putative Roles for Peptidylarginine Deiminases in COVID-19.International journal of molecular sciences · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Meiyan LiuDepartment of Internal Medicine, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150040, P.R. China.
Yang QuDepartment of Internal Medicine, The Second Hospital of Heilongjiang Province, Harbin, Heilongjiang 150010, P.R. China.
Xue TengDepartment of Pharmacy, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150040, P.R. China.
Ying XingDepartment of Internal Medicine, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150040, P.R. China.
Dandan LiDepartment of Internal Medicine, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150040, P.R. China.
Chunhong LiDepartment of Internal Medicine, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150040, P.R. China.
Li CaiDepartment of Internal Medicine, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150040, P.R. China.
Third Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is a complex disease involving multiple genetic and phenotypic alterations. As a histone modification enzyme, protein‑arginine deiminase type‑4 (PADI4) and its downstream signaling have been studied in the progression of a variety of types of human cancer, but data on PADI4‑mediated posttranslational modification in lung cancer are lacking. The aim of present study was to evaluate the expression of PADI4 and its associated molecular signaling in lung cancer metastasis. The results of the present study indicated that PADI4 was overexpressed in lung cancer cells, while knockdown of PADI4 could lead to attenuation of the lung cancer cell invasion and migration phenotype, which was further verified by determining the epithelial‑mesenchymal transition (EMT) marker proteins. Additionally, it was demonstrated that stable knockdown of PADI4 in A549 lung cancer cells resulted in a striking reduction of the EMT‑associated Snail1/mothers against decapentaplegic homolog 3/4 transcriptional complex, which was consistent with alterations in migratory and invasive phenotypes of A549 lung cancer cells. Therefore, PADI4‑mediated EMT transition is proposed to represent a novel mechanism underlying the epigenetic and phenotypic alterations in lung cancer cells, and the PADI4 associated signaling pathway may be a therapeutic target for treating lung cancer in a clinical setting.

Indexed as

A549 CellsBiomarkers, TumorCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionGene ExpressionGene Knockdown TechniquesHumansImmunohistochemistryLung NeoplasmsProtein-Arginine DeiminasesProtein-Arginine Deiminase Type 4RNA InterferenceRNA, Small InterferingSignal TransductionBiomarkers, TumorPADI4 protein, humanProtein-Arginine DeiminasesProtein-Arginine Deiminase Type 4RNA, Small Interfering

Identifiers

PMID30816464
PMCPMC6423585
OpenAlexW2917133087

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.