Evidence map›Paper›PMID 39249547›Full record

ArticleFunctional & integrative genomics2024

Long non-coding RNA MAGEA4-AS1 binding to p53 enhances MK2 signaling pathway and promotes the proliferation and metastasis of oral squamous cell carcinoma.

Xiaoxiao Wei, Zhangfu Li, Heng Zheng, Xiaolian Li, Yuntao Lin, Hongyu Yang, Yuehong Shen

Abstract read
In one paragraph

Article in Functional & integrative genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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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.

Xiaoxiao Wei *Peking University Shenzhen Hospital Clinical College, The Fifth School of Clinical Medicine, Anhui Medical University, Hefei, Anhui, 230032, China.
Zhangfu Li *Department of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China.
Heng ZhengPeking University Shenzhen Hospital Clinical College, The Fifth School of Clinical Medicine, Anhui Medical University, Hefei, Anhui, 230032, China.
Xiaolian LiDepartment of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China.
Yuntao LinDepartment of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China.
Hongyu YangPeking University Shenzhen Hospital Clinical College, The Fifth School of Clinical Medicine, Anhui Medical University, Hefei, Anhui, 230032, China. yanghongyu@ahmu.edu.cn.
Yuehong ShenPeking University Shenzhen Hospital Clinical College, The Fifth School of Clinical Medicine, Anhui Medical University, Hefei, Anhui, 230032, China. yhshen@pkuszh.com.

Funding

Shenzhen Clinical Research Center for Oral Diseases 20210617170745001Shenzhen Fund for Guangdong Provincial High-level Clinical Key Specialties No. SZGSP008Shenzhen High-level Hospital Construction Fund, Peking University Shenzhen Hospital Scientific Research Fund KYQD2023253Shenzhen Science and Technology Program JCYJ20200109140208058Shenzhen Science and Technology Program JCYJ20220531094216037the Sanming Project of Medicine in Shenzhen SZSM 202111012
6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) regulate the occurrence, development and progression of oral squamous cell carcinoma (OSCC). We elucidated the expression features of MAGEA4-AS1 in patients with OSCC and its activity as an OSCC biomarker. Furthermore, the impact of up-regulation of MAGEA4-AS1 on the cellular behaviors (proliferation, migration and invasion) of OSCC cells and intrinsic signal mechanisms were evaluated. Firstly, we analyzed MAGEA4-AS1 expression data in The Cancer Genome Atlas (TCGA) OSCC using a bioinformatics approach and in 45 pairs of OSCC tissues using qPCR. Then CCK-8, ethynyl deoxyuridine, colony formation, transwell and wound healing assays were conducted to assess changes in the cell proliferation, migration and invasion protential of shMAGEA4-AS1 HSC3 and CAL27 cells. The RNA sequence of MAGEA4-AS1 was identified using the rapid amplification of cDNA ends (RACE) assay. And whole-transcriptome sequencing was used to identify MAGEA4-AS1 affected genes. Additionally, dual-luciferase reporter system, RNA-binding protein immunoprecipitation (RIP), and rescue experiments were performed to clarify the role of the MAGEA4-AS1-p53-MK2 signaling pathway. As results, we found MAGEA4-AS1 was up-regulated in OSCC tissues. We identified a 418 nucleotides length of the MAGEA4-AS1 transcript and it primarily located in the cell nucleus. MAGEA4-AS1 stable knockdown weakened the proliferation, migration and invasion abilities of OSCC cells. Mechanistically, p53 protein was capable to activate MK2 gene transcription. RIP assay revealed an interaction between p53 and MAGEA4-AS1. MK2 up-regulation in MAGEA4-AS1 down-regulated OSCC cells restored MK2 and epithelial-to-mesenchymal transition related proteins' expression levels. In conclusion, MAGEA4-AS1-p53 complexes bind to MK2 promoter, enhancing the transcription of MK2 and activating the downstream signaling pathways, consequently promoting the proliferation and metastasis of OSCC cells. MAGEA4-AS1 may serve as a diagnostic marker and therapeutic target for OSCC patients.

Indexed as

Cell MovementCell ProliferationIntracellular Signaling Peptides and ProteinsMouth NeoplasmsProtein Serine-Threonine KinasesRNA, Long NoncodingSignal TransductionTumor Suppressor Protein p53Carcinoma, Squamous CellCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMAP-Kinase-Activated Kinase 2Neoplasm MetastasisIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2Protein Serine-Threonine KinasesRNA, Long NoncodingTP53 protein, humanTumor Suppressor Protein p53EMTlncRNAsMAGEA4-AS1MK2p53Transcription regulation

Identifiers

PMID39249547
PMCPMC11384635

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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.