Integration of ETS2 Expression Data in Multi-Omics Cancer Profiling

Carsten Menden^*
*Correspondence: Carsten Menden, Department of Dermatology and Venereology, University of Freiburg, Freiburg, Germany, Email:

Introduction

Advancements in cancer research have increasingly embraced multi-omics approaches to understand the molecular heterogeneity and complexity of tumorigenesis. By integrating data from genomics, transcriptomics, epigenomics, proteomics, and metabolomics, researchers aim to uncover the dynamic interplay between genetic regulation and phenotypic manifestation in cancer. One gene of particular interest in these integrative analyses is ETS2, a member of the ETS family of transcription factors. ETS2 is implicated in diverse cellular processes, including proliferation, differentiation, apoptosis, and inflammationâ??functions that are frequently dysregulated in cancer. The inclusion of ETS2 expression data in multi-omics cancer profiling has the potential to elucidate novel mechanisms of tumor progression and inform biomarker discovery and targeted therapy development [1].

Description

ETS2 is a transcription factor encoded on chromosome 21q22 and is often overexpressed or functionally altered in various cancers. Its regulatory roles are context-dependent, acting either as an oncogene or a tumor suppressor depending on the tumor type and cellular environment. Multi-omics profiling enables the comprehensive evaluation of ETS2â??s role by examining not only its mRNA expression but also its epigenetic regulation, post-translational modifications, protein-protein interactions, and impact on downstream metabolic and signaling pathways. Integrative analyses using datasets such as those from The Cancer Genome Atlas (TCGA) or the International Cancer Genome Consortium (ICGC) have revealed that ETS2 expression correlates with tumor grade, immune infiltration, and therapy response across several cancer types, including breast, lung, colorectal, and hematologic malignancies [2]. At the transcriptomic level, ETS2 expression is often co-regulated with genes involved in cell cycle progression, inflammatory signaling, and Epithelial-Mesenchymal Transition (EMT). When integrated with DNA methylation and histone modification data, studies have shown that ETS2 expression is frequently regulated by epigenetic mechanisms. Hypermethylation of ETS2 promoter regions has been observed in certain cancers, leading to reduced expression and impaired tumor suppressor function. Conversely, in tumors where ETS2 acts as an oncogene, hypomethylation or enhancer activation by transcriptional co-activators increases its expression, contributing to uncontrolled cell proliferation and metastasis [3].

Proteomic data further enrich this analysis by detailing the post-translational modifications of ETS2, such as phosphorylation by kinases in the MAPK or JNK pathways, which alter its transcriptional activity and protein stability. These modifications may serve as functional switches that determine whether ETS2 exerts pro- or anti-tumorigenic effects. Integration of proteomic profiles has also revealed ETS2â??s interactions with other transcription factors and co-regulators, such as p53, RUNX1, and AP-1, highlighting its role in complex transcriptional networks that modulate cancer cell behavior. Metabolomic studies, although less frequently linked to transcription factors, have started to explore ETS2's downstream metabolic consequences. ETS2-mediated transcriptional programs often influence metabolic genes involved in glycolysis, oxidative phosphorylation, and lipid metabolism, suggesting a role in shaping the metabolic landscape of cancer cells. This connection between transcriptional regulation and metabolism adds another layer to the understanding of ETS2 function and its potential as a therapeutic target [4]. The integration of ETS2 data across these omics layers facilitates the identification of molecular subtypes of cancer with distinct ETS2-driven pathways. For example, high ETS2 expression in certain breast cancer subtypes correlates with immune evasion signatures and poor prognosis, while in colorectal cancer, ETS2 downregulation is associated with loss of differentiation and increased tumor aggressiveness. Such insights support the use of ETS2 as a potential biomarker for patient stratification, guiding personalized therapy and prognosis assessment [5].

Conclusion

In conclusion, the integration of ETS2 expression data within multi-omics cancer profiling reveals the complex and context-dependent roles of this transcription factor in oncogenesis. By bridging genomic, epigenomic, transcriptomic, proteomic, and metabolomic data, researchers can gain a more holistic view of ETS2â??s function and its contribution to tumor biology. These insights are not only critical for understanding cancer mechanisms but also for developing targeted interventions and improving diagnostic precision. As multi-omics technologies continue to evolve, ETS2 remains a valuable molecular node whose regulation and impact merit ongoing investigation in the era of precision oncology.

Acknowledgment

None.

Conflict of Interest

None.

References

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