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Updated: Jul 19, 2025

Experimental Melanoma Immunotherapy Model Using Tumor Vaccination with a Hematopoietic Cytokine
Published on: February 24, 2023
Transcriptomic characterization revealed that METTL7A inhibits melanoma progression via the p53 signaling pathway and
Duoli Zhang1, Tao Zou1, Qingsong Liu2
1Department of Pharmacology, School of Pharmacy, Southwest Medical University, Laboratory of Molecular Pharmacology, Luzhou, China.
Abstract:
METTL7A is a protein-coding gene expected to be associated with methylation, and its expression disorder is associated with a range of diseases. However, few research have been carried out to explore the relationship between METTL7A and tumor malignant phenotype as well as the involvement potential mechanism. We conducted our research via a combination of silico analysis and molecular biology techniques to investigate the biological function of METTL7A in the progression of cancer. Gene expression and clinical information were extracted from the TCGA database to explore expression variation and prognostic value of METTL7A. In vitro, CCK8, transwell, wound healing and colony formation assays were conducted to explore the biological functions of METT7A in cancer cell. GSEA was performed to explore the signaling pathway involved in METTL7A and validated via western blotting. In conclusion, METTL7A was downregulated in most cancer tissues and its low expression was associated with shorter overall survival. In melanoma, METTL7A downregulation was associated with poorer clinical staging, lower levels of TIL infiltration, higher IC50 levels of chemotherapeutic agents, and poorer immunotherapy outcomes. QPCR results confirm that METTL7A is down-regulated in melanoma cells. Cell function assays showed that METTL7A knockdown promoted proliferation, invasion, migration and clone formation of melanoma cells. Mechanistic studies showed that METTL7A inhibits tumorigenicity through the p53 signaling pathway. Meanwhile, METTL7A is also a potential immune regulatory factor.
Insights
Methylthiotranspherase like 7A (METTL7A) gene downregulation correlates with poorer cancer outcomes and promotes melanoma progression. METTL7A inhibits tumor growth via the p53 pathway and influences immune response.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genomics
Background:
- METTL7A (Methylthiotranspherase like 7A) is linked to methylation and diseases, but its role in cancer malignancy and mechanisms remains unclear.
- Understanding METTL7A's function is crucial for cancer research and therapeutic development.
Purpose of the Study:
- To investigate the biological function and prognostic value of METTL7A in cancer progression.
- To elucidate the underlying molecular mechanisms of METTL7A's involvement in tumorigenesis, particularly in melanoma.
Main Methods:
- Bioinformatic analysis of TCGA database for gene expression and clinical correlation.
- In vitro assays (CCK8, Transwell, wound healing, colony formation) to assess METTL7A's functional impact on cancer cells.
- Gene Set Enrichment Analysis (GSEA) and Western Blotting for pathway analysis.
Main Results:
- METTL7A is downregulated in most cancers, with low expression linked to shorter survival.
- In melanoma, reduced METTL7A correlates with advanced stage, low tumor-infiltrating lymphocytes (TILs), chemoresistance, and poor immunotherapy response.
- METTL7A knockdown enhances melanoma cell proliferation, invasion, migration, and colony formation, acting through the p53 signaling pathway.
Conclusions:
- METTL7A functions as a tumor suppressor, inhibiting tumorigenicity via the p53 pathway.
- METTL7A downregulation is a marker for poor prognosis in various cancers, especially melanoma.
- METTL7A holds potential as a prognostic biomarker and immune regulatory factor in cancer treatment.
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