Evidence map›Paper›PMID 30683132›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

PRDM16 functions as a suppressor of lung adenocarcinoma metastasis.

Liang-Ru Fei, Wen-Jing Huang, Yuan Wang, Lei Lei, Zhi-Han Li, Yi-Wen Zheng, Zhao Wang, Mai-Qing Yang, Chen-Chen Liu, Hong-Tao Xu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

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  19. MiR-96-5p Facilitates Lung Adenocarcinoma Cell Phenotypes by Inhibiting FHL1.Computational and mathematical methods in medicine · 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

10 authors at 1 institution in 1 country.

Liang-Ru FeiDepartment of Pathology, College of Basic Medical Sciences and the First Affiliated Hospital, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, 110122, People's Republic of China.
Wen-Jing HuangDepartment of Pathology, College of Basic Medical Sciences and the First Affiliated Hospital, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, 110122, People's Republic of China.
Yuan WangDepartment of Pathology, College of Basic Medical Sciences and the First Affiliated Hospital, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, 110122, People's Republic of China.
Lei LeiDepartment of Pathology, College of Basic Medical Sciences and the First Affiliated Hospital, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, 110122, People's Republic of China.
Zhi-Han LiDepartment of Pathology, College of Basic Medical Sciences and the First Affiliated Hospital, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, 110122, People's Republic of China.
Yi-Wen ZhengDepartment of Pathology, College of Basic Medical Sciences and the First Affiliated Hospital, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, 110122, People's Republic of China.
Zhao WangDepartment of Pathology, College of Basic Medical Sciences and the First Affiliated Hospital, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, 110122, People's Republic of China.
Mai-Qing YangDepartment of Pathology, College of Basic Medical Sciences and the First Affiliated Hospital, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, 110122, People's Republic of China.
Chen-Chen LiuDepartment of Pathology, College of Basic Medical Sciences and the First Affiliated Hospital, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, 110122, People's Republic of China.
Hong-Tao XuDepartment of Pathology, College of Basic Medical Sciences and the First Affiliated Hospital, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, 110122, People's Republic of China. xuht@cmu.edu.cn.ORCID http://orcid.org/0000-0001-5062-3108
First Hospital of China Medical University · CN

Funding

National Natural Science Foundation of China 81372497Program for Liaoning Excellent Talents in University LR2015067
6 · The paper itself

Abstract

backgroundThe transcription factor PR domain containing 16 (PRDM16) is known to play a significant role in the determination and function of brown and beige fat. However, the role of PRDM16 in tumor biology has not been well addressed. Here we investigated the impact of PRDM16 on tumor growth and metastasis in lung cancer.

methodsUALCAN database, immunoblotting and immunohistochemistry analysis were used to assess PRDM16 expression in lung cancer patients. Kaplan-Meier plotter database was used to analyze the overall survival of patients with lung cancer stratified by PRDM16 expression. PRDM16 overexpression and knockdown experiments were conducted to assess the effects of PRDM16 on growth and metastasis in vitro and in vivo, and its molecular mechanism was investigated in lung adenocarcinoma cells by chromatin immunoprecipitation-sequencing (ChIP-Seq), real time-quantitative PCR (RT-qPCR), luciferase assay, xenograft models and rescue experiments.

resultsPRDM16 was downregulated in lung adenocarcinomas, and its expression level correlated with key pathological characteristics and prognoses of lung adenocarcinoma patients. Overexpressing PRDM16 inhibited the epithelial-to-mesenchymal transition (EMT) of cancer cells both in vivo and in vitro by repressing the transcription of Mucin-4 (MUC4), one of the regulators of EMT in lung adenocarcinomas. Furthermore, deleting the PR domain from PRDM16 increased the transcriptional repression of MUC4 by exhibiting significant differences in histone modifications on its promoter.

conclusionsOur findings demonstrate a critical interplay between transcriptional and epigenetic modifications during lung adenocarcinoma progression involving EMT of cancer cells and suggest that PRDM16 is a metastasis suppressor and potential therapeutic target for lung adenocarcinomas.

Indexed as

Adenocarcinoma of LungAnimalsCell Line, TumorCell MovementCell ProliferationDisease-Free SurvivalDNA-Binding ProteinsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMaleMiceMucin-4Neoplasm MetastasisDNA-Binding ProteinsMUC4 protein, humanMucin-4PRDM16 protein, humanTranscription FactorsEMTLung cancerMUC4PRDM16

Identifiers

PMID30683132
PMCPMC6347838
OpenAlexW2920064413

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.