ArticleHistology and histopathology2024
E2F1-EP300 co-activator complex potentiates immune escape in nasopharyngeal carcinoma through the mediation of MELK.
Article in Histology and histopathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 1 citations in OpenAlex.
- Article
- The chromatin remodeling factors EP300 and TRRAP are novel SMYD3 interactors involved in the emerging 'nonmutational epigenetic reprogramming' cancer hallmark.Computational and structural biotechnology journal · 2023Article
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3 authors at 1 institution in 1 country.
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Abstract
backgroundNasopharyngeal carcinoma (NPC) is characterized by a highly suppressive microenvironment that protects tumor cells against immune attack and facilitates tumor progression. MELK is upregulated in various tumors, whereas its function in the immune escape remains largely unknown. In this study, we investigated the role of MELK during immune escape in NPC.
methodsDifferentially expressed genes were filtered using GEO datasets and PPI network analysis. NPC cell colony formation and motility were examined, and the impact of CD8⁺ T cells on NPC cells was evaluated. A xenograft model was constructed to detect the growth of tumor cells and the T-cell phenotype of tumor infiltration. ChIP-qPCR and dual-luciferase assays were used to verify the transcriptional regulation of MELK by EP300/E2F1.
findingsMELK was overexpressed in NPC, and sh-MELK suppressed the clonogenic ability, migration, and invasion of NPC cells and promoted the killing effects of CD8⁺ T cells. These
interpretationEP300 coordinated with E2F1 to promote the transcription of MELK which promoted the growth of NPC cells and repressed the killing effect of CD8⁺ T cells. Blockage of MELK may be a potential way to suppress the immune escape of NPC cells.
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