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

## TL;DR

This study identifies MYBL2 as a potential biomarker for uterine corpus endometrial carcinoma, linking its overexpression to disease progression and immune interactions.

## Contribution

The study establishes MYBL2 as a novel biomarker and therapeutic target in uterine corpus endometrial carcinoma through bioinformatics and clinical validation.

## Key findings

- MYBL2 is significantly upregulated in uterine corpus endometrial carcinoma compared to normal tissues.
- Elevated MYBL2 expression correlates with advanced tumor grade and stage, suggesting a role in disease progression.
- MYBL2 is associated with immune cell infiltration and chemokine expression, indicating immune modulation.

## Abstract

Endometrial 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).

We 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.

MYBL2 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.

This 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.