Evidence map›Paper›PMID 34039308›Full record

ArticleBMC cancer2021

Evaluation of clinical value and potential mechanism of MTFR2 in lung adenocarcinoma via bioinformatics.

Cheng Chen, Yang Tang, Wen-Dong Qu, Xu Han, Jie-Bin Zuo, Qing-Yong Cai, Gang Xu, Yong-Xiang Song, Xi-Xian Ke

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2021. 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
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

14 citing papers in PubMed, 18 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

9 authors at 1 institution in 1 country.

Cheng ChenDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Yang TangDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Wen-Dong QuDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Xu HanDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Jie-Bin ZuoDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Qing-Yong CaiDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Gang XuDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Yong-Xiang SongDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China. songtang2004@163.com.
Xi-Xian KeDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China. kexixian@zmu.edu.cn.
Zunyi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMitochondrial fission regulator 2 (MTFR2) was involved in the progression and development of various cancers. However, the relationship between MTFR2 with lung adenocarcinoma (LUAD) had not been reported. Herein, this study analyzed the clinical significance and potential mechanisms of MTFR2 in LUAD via bioinformatics tools.

resultsWe found that the level of MTFR2 was increased, and correlated with sex, age, smoking history, neoplasm staging, histological subtype and TP53 mutation status in LUAD patients. Kaplan-Meier survival analysis showed LUAD patients with increased MTFR2 had a poor prognosis. In addition, univariate COX regression analysis showed neoplasm staging, T stage, distant metastasis and MTFR2 level were risk factors for the prognosis of LUAD. A total of 1127 genes were coexpressed with MTFR2, including 840 positive and 208 negative related genes. KEGG and GSEA found that MTFR2 participated in the progression of LUAD by affecting cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other mechanisms. The top 10 coexpressed genes, namely CDK1, CDC20, CCNB1, PLK1, CCNA2, AURKB, CCNB2, BUB1B, MAD2L1 and BUB1 were highly expressed, and were associated with poor prognosis in LUAD.

conclusionsConsequently, we elucidated MTFR2 was a biomarker for diagnosis and poor prognosis in LUAD, and might participate in the progression of LUAD via affecting cell cycle, DNA replication, homologous recombination and p53 signaling pathway.

Indexed as

Adenocarcinoma of LungAdultAgedAged, 80 and overBiomarkers, TumorComputational BiologyDatasets as TopicDisease-Free SurvivalFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateLungLung NeoplasmsMaleBiomarkers, TumorMitochondrial ProteinsMTFR2 protein, humanBioinformaticsBiomarkerLung adenocarcinomaMTFR2Prognosis

Identifiers

PMID34039308
PMCPMC8157440
OpenAlexW3118549967

What Socratic 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 Socratic graph.