Evidence map›Paper›PMID 37667226›Full record

ArticleBMC cancer2023

MALAT1-regulated gene expression profiling in lung cancer cell lines.

Jungwook Roh, Boseong Kim, Mijung Im, Wonyi Jang, Yeonsoo Chae, JiHoon Kang, BuHyun Youn, Wanyeon Kim

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

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  15. Expression profile of serum LncRNAsNon-coding RNA research · 2024
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  17. Identification ofCancer genomics & proteomics
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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

8 authors at 3 institutions in 2 countries.

Jungwook Roh *Department of Science Education, Korea National University of Education, Cheongju-si, 28173, Chungbuk, Republic of Korea.
Boseong Kim *Department of Science Education, Korea National University of Education, Cheongju-si, 28173, Chungbuk, Republic of Korea.
Mijung ImDepartment of Science Education, Korea National University of Education, Cheongju-si, 28173, Chungbuk, Republic of Korea.
Wonyi JangDepartment of Science Education, Korea National University of Education, Cheongju-si, 28173, Chungbuk, Republic of Korea.
Yeonsoo ChaeDepartment of Science Education, Korea National University of Education, Cheongju-si, 28173, Chungbuk, Republic of Korea.
JiHoon KangDepartment of Hematology and Medical Oncology, Winship Cancer Institute of Emory, Emory University School of Medicine, Atlanta, GA, 30322, USA.
BuHyun YounDepartment of Biological Sciences, Pusan National University, Busan, 46241, Republic of Korea.
Wanyeon KimDepartment of Science Education, Korea National University of Education, Cheongju-si, 28173, Chungbuk, Republic of Korea. wykim82@knue.ac.kr.
Korea National University of Education · KREmory University · USPusan National University · KR

Funding

National Research Foundation of Korea 2019R1C1C1009423National Research Foundation of Korea 2022R1A6A3A13072277
6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) is the most common type of lung cancer and has a poor prognosis. Identifying biomarkers based on molecular mechanisms is critical for early diagnosis, timely treatment, and improved prognosis of lung cancer. MALAT1 has been reported to have overexpressed and tumor-promoting functions in NSCLC. It has been proposed as a potential biomarker for the diagnosis and prognosis of cancer. Therefore, this study was conducted to profile the changes in gene expression according to the regulation of expression of MALAT1 in NSCLC cell lines and to investigate the correlation through bioinformatic analysis of differentially expressed genes (DEGs).

methodsMALAT1 expression levels were measured using RT-qPCR. The biological functions of MALAT1 in NSCLC were analyzed by cell counting, colony forming, wound-healing, and Transwell invasion assays. In addition, gene expression profiling in response to the knockdown of MALAT1 was analyzed by transcriptome sequencing, and differentially expressed genes regulated by MALAT1 were performed by GO and KEGG pathway enrichment analyses. Bioinformatic databases were used for gene expression analysis and overall survival analysis.

resultsComparative analysis versus MALAT1 expression in MRC5 cells (a normal lung cell line) and the three NSCLC cell lines showed that MALAT1 expression was significantly higher in the NSCLC cells. MALAT1 knockdown decreased cell survival, proliferation, migration, and invasion in all three NSCLC cell lines. RNA-seq analysis of DEGs in NSCLC cells showed 198 DEGs were upregulated and 266 DEGs downregulated by MALAT1 knockdown in all three NSCLC cell lines. Survival analysis on these common DEGs performed using the OncoLnc database resulted in the selection of five DEGs, phosphoglycerate mutase 1 (PGAM1), phosphoglycerate mutase 4 (PGAM4), nucleolar protein 6 (NOL6), nucleosome assembly protein 1 like 5 (NAP1L5), and sestrin1 (SESN1). The gene expression levels of these selected DEGs were proved to gene expression analysis using the TNMplot database.

conclusionMALAT1 might function as an oncogene that enhances NSCLC cell survival, proliferation, colony formation, and invasion. RNA-seq and bioinformatic analyses resulted in the selection of five DEGs, PGAM1, PGAM4, NOL6, NAP1L5, and SESN1, which were found to be closely related to patient survival and tumorigenesis. We believe that further investigation of these five DEGs will provide valuable information on the oncogenic role of MALAT1 in NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsRNA, Long NoncodingGene Expression ProfilingHumansPhosphoglycerate MutaseMALAT1 long non-coding RNA, humanPhosphoglycerate MutaseRNA, Long NoncodingBioinformaticsLncRNALung CancerMALAT1NSCLC

Identifiers

PMID37667226
PMCPMC10476395
OpenAlexW4386413629

What OpenQuestion holds

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LicenceCC BY
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.