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Knockdown of Methylation-Related Gene MBD2 Blocks Cell Growth by Upregulating p21 Expression in Head and Neck
Ting Cao1, Xia Shen2, Fei Pei3
1Center for Medical Research and Innovation, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, China.
Background:
Methyl-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.
Aims:
This 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.
Methods:
We 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.
Results:
MBD2 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.
Conclusion:
These 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.
Insights
Methyl-CpG-binding domain 2 (MBD2) is overexpressed in head and neck squamous cell carcinoma (HNSCC), driving tumor progression. Inhibiting MBD2 or using 5-azacytidine upregulates p21, suppressing HNSCC growth and viability.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Methyl-CpG-binding domain 2 (MBD2) regulates gene transcription via methylated DNA, impacting tumor progression.
- The specific role of MBD2 in head and neck squamous cell carcinoma (HNSCC) requires further elucidation.
Purpose of the Study:
- To evaluate the clinical significance of MBD2 expression in HNSCC.
- To investigate MBD2's functional role in HNSCC progression, including its regulation of p21 and cellular proliferation.
Main Methods:
- Analyzed MBD2 expression, clinicopathological features, and survival data from UALCAN, TCGA, and cBioPortal databases.
- Conducted in vitro experiments involving MBD2 knockdown and 5-azacytidine treatment in HNSCC cell lines.
- Assessed p21 expression, cell proliferation, and viability following MBD2 manipulation and treatment.
Main Results:
- MBD2 overexpression in HNSCC correlated with reduced overall survival and disease-free survival.
- Both MBD2 knockdown and 5-azacytidine treatment increased p21 expression in HNSCC cells.
- These interventions significantly inhibited HNSCC cell proliferation and viability.
Conclusions:
- MBD2 knockdown suppresses HNSCC growth by enhancing p21 expression.
- MBD2 functions as an oncogene in HNSCC and presents a potential prognostic biomarker and therapeutic target.
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