Apoprotein E methylation is correlated with immune microenvironment in hepatocellular carcinoma.
Acta Oncol
; 62(6): 550-559, 2023 Jun.
Article
en En
| MEDLINE
| ID: mdl-37352133
ABSTRACT
BACKGROUND:
We aimed to evaluate the correlation of apoprotein E (APOE) transcription and its methylation with immune microenvironment in HCC patients. MATERIAL ANDMETHODS:
The expression profiles of APOE transcription, APOE methylation, and APOE protein were investigated via comprehensive bioinformatic analyses. After that, the association between the immune activation of HCC and APOE transcription and methylation were analyzed. Finally, the prognostic role and immune correlation of the APOE protein in 92 HCC individuals was determined.RESULTS:
Based on data from TCGA, GEO, and ICGC datasets, the APOE mRNA was differentially expressed in HCC tissues compared with normal liver tissues. Further, APOE methylation was down-regulated in HCC tissues compared to normal liver tissues. APOE methylation was negatively correlated with APOE transcription in HCC (r=-0.52, p < 0.0001). Based on APOE methylation, the HCC patients were stratified into hypermethylation and hypomethylation subgroups as they exhibited different immune activation statuses. Further, HCC individuals with APOE hypermethylation had a closer immune correlation than those with hypomethylation. Notably, APOE transcription was associated with weak immune infiltrates and activation. Finally, over-expression of the APOE protein was correlated with better survival outcomes, but not correlated with PD-1 or CTLA4 protein in HCC revealed by immunohistochemistry.CONCLUSION:
APOE methylation had a closer correlation with immune cells than APOE mRNA, indicating that APOE methylation might play an important role in immune regulation in HCC.Palabras clave
Texto completo:
1
Colección:
01-internacional
Asunto principal:
Carcinoma Hepatocelular
/
Neoplasias Hepáticas
Tipo de estudio:
Prognostic_studies
Límite:
Humans
Idioma:
En
Revista:
Acta Oncol
Asunto de la revista:
NEOPLASIAS
Año:
2023
Tipo del documento:
Article