AUTHOR=Lu Jiaoyun , Luo Furong 

TITLE=MYB Proto-Oncogene Like 2 identified as a biomarker for uterine corpus endometrial carcinoma: evidence from bioinformatics and clinical validation

JOURNAL=Frontiers in Oncology

VOLUME=Volume 15 - 2025

YEAR=2025

URL=https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2025.1595485

DOI=10.3389/fonc.2025.1595485

ISSN=2234-943X

ABSTRACT=BackgroundEndometrial carcinoma (EC) is the sixth most prevalent malignancy among women globally, posing a significant clinical challenge due to limited therapeutic options for advanced or recurrent cases. The identification of novel prognostic biomarkers and therapeutic targets is crucial for improving patient outcomes. This study aimed to investigate the multifaceted roles of MYB Proto-Oncogene Like 2 (MYBL2) in uterine corpus endometrial carcinoma (UCEC).MethodsWe employed multiple bioinformatics algorithms (GEPIA, TCGA, TIMER2.0) to analyze MYBL2 expression across different cancer types and in UCEC specifically. Expression patterns were validated using quantitative real-time PCR (qPCR) on clinical samples. Epigenetic analyses focused on promoter methylation status, and immune infiltration patterns were assessed using MethSurv, CIBERSORT and TIMER2.0. Drug sensitivity profiling was performed using the CPADS web platform.ResultsMYBL2 was found to be significantly upregulated in UCEC tumors compared to normal tissues. Elevated MYBL2 expression correlated with advanced histologic grade and clinical stage, indicating its potential as a biomarker for disease progression. Epigenetic analysis revealed promoter hypomethylation in tumors, suggesting a regulatory mechanism driving MYBL2 overexpression. MYBL2 demonstrated dynamic interactions with the tumor immune microenvironment, including associations with immune cell infiltration patterns and co-expression with immune checkpoint molecules and chemokines. Drug sensitivity profiling highlighted differential therapeutic responses linked to MYBL2 expression levels.ConclusionThis study establishes MYBL2 as a critical regulator of UCEC progression, bridging epigenetic dysregulation, immune modulation, and clinical outcomes. The findings provide a foundation for exploring MYBL2-targeted strategies in precision immunotherapy and personalized therapeutic interventions.