Evidence map›Paper›PMID 39676597›Full record

ArticleCancer reports (Hoboken, N.J.)2024

Knockdown of Methylation-Related Gene MBD2 Blocks Cell Growth by Upregulating p21 Expression in Head and Neck Squamous Cell Carcinoma.

Ting Cao, Xia Shen, Fei Pei, Taogeng Jiang, Jun Zhang, Hong Zhou

Abstract read
In one paragraph

Article in Cancer reports (Hoboken, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Ting CaoCenter for Medical Research and Innovation, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, China.
Xia ShenDepartment of Otolaryngology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, China.
Fei PeiDepartment of Otolaryngology, Shidong Hospital, Yangpu District, Shidong Hospital Affiliated to University of Shanghai for Science and Technology, Shanghai, China.
Taogeng JiangDepartment of Otolaryngology, Shidong Hospital, Yangpu District, Shidong Hospital Affiliated to University of Shanghai for Science and Technology, Shanghai, China.
Jun ZhangDepartment of Otolaryngology, Shidong Hospital, Yangpu District, Shidong Hospital Affiliated to University of Shanghai for Science and Technology, Shanghai, China.
Hong ZhouDepartment of Otolaryngology, Shidong Hospital, Yangpu District, Shidong Hospital Affiliated to University of Shanghai for Science and Technology, Shanghai, China.ORCID 0000-0002-1484-500X

Funding

Scientific Research Foundation provided by Pudong Hospital affiliated to Fudan University YJ2021-03Shanghai Sailing Program 21YF1441800
6 · The paper itself

Abstract

backgroundMethyl-CpG-binding domain 2 (MBD2) attaches to methylated DNA, which mediates methylated gene transcription, leading to gene silencing and affecting tumor progression. The molecular mechanisms of MBD2 in head and neck squamous cell carcinoma (HNSCC) remain insufficiently characterized.

aimsThis study sought to assess the clinical relevance of MBD2 expression in HNSCC, with a particular focus on elucidating its functional role in tumor progression and its regulatory influence on p21 expression and cellular proliferation.

methodsWe analyzed the relationships between MBD2 expression, clinicopathological features, and survival outcomes in HNSCC patients using data from the UALCAN, TCGA, and cBioPortal databases. The functional role of MBD2 in HNSCC was further investigated through in vitro experiments. p21 expression was assessed using western blotting and qRT-PCR in TU212 and AMC-HN8 cells. These cells were treated with either shRNA targeting MBD2, 5-azacytidine (5-Aza), or a combination of shRNA MBD2 and 5-Aza. Additionally, cell proliferation and viability were measured in each treatment group.

resultsMBD2 was found to be frequently overexpressed in HNSCC tissues, and its altered expression was significantly associated with reduced overall survival (OS) and disease-free survival (DFS). Both shRNA-mediated MBD2 knockdown and 5-Aza treatment increased p21 expression in HNSCC cells, exhibiting similar functions with additive effects. Furthermore, both treatments significantly inhibited cell proliferation and viability.

conclusionThese results indicated that shRNA-mediated MBD2 knockdown suppresses HNSCC cell growth by upregulating p21 expression. In addition to its role as an oncogene, MBD2 may serve as a prognostic biomarker and therapeutic target for HNSCC patients.

Indexed as

Cell ProliferationCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsDNA MethylationGene Expression Regulation, NeoplasticHead and Neck NeoplasmsSquamous Cell Carcinoma of Head and NeckAgedAzacitidineBiomarkers, TumorCell Line, TumorFemaleGene Knockdown TechniquesHumansMaleMiddle AgedAzacitidineBiomarkers, TumorCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsMBD2 protein, human5‐azacytidine (5‐Aza)head and neck squamous cell carcinoma (HNSCC)methyl‐CpG‐binding domain 2 (MBD2)p21prognosis

Identifiers

PMID39676597
PMCPMC11647173

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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.