ORIGINAL RESEARCH article
Front. Oncol.
Sec. Cancer Immunity and Immunotherapy
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1595485
This article is part of the Research TopicHarnessing Molecular Insights for Enhanced Drug Sensitivity and Immunotherapy in CancerView all 31 articles
MYB Proto-Oncogene Like 2 Identified as a Biomarker for Uterine Corpus Endometrial Carcinoma: evidence from Bioinformatics and Clinical Validation
Provisionally accepted
Jiaoyun Lu1
Furong Luo2*- 1Department of Oncology, Xi’an NO.3 Hospital, the Affiliated Hospital of Northwest University, Xi'an, China
- 2Department of Traditional Chinese Medicine, Xi’an NO.3 Hospital, the Affiliated Hospital of Northwest University, Xi'an, China
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Background: 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). Methods: 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. Results: 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. Conclusion: 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.
Keywords: MYBL2, Uterine corpus endometrial carcinoma, prognosis, Immune infiltration, biomarker
Received: 18 Mar 2025; Accepted: 23 Apr 2025.
Copyright: © 2025 Lu and Luo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Furong Luo, Department of Traditional Chinese Medicine, Xi’an NO.3 Hospital, the Affiliated Hospital of Northwest University, Xi'an, China
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