Related Experiment Video
Updated: May 7, 2026

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
Published on: June 27, 2020
Molecular mechanisms of ETS transcription factor-mediated tumorigenesis
Adwitiya Kar1, Arthur Gutierrez-Hartmann
1Cancer Biology Training Program .
Abstract:
The E26 transformation-specific (ETS) family of transcription factors is critical for development, differentiation, proliferation and also has a role in apoptosis and tissue remodeling. Changes in expression of ETS proteins therefore have a significant impact on normal physiology of the cell. Transcriptional consequences of ETS protein deregulation by overexpression, gene fusion, and modulation by RAS/MAPK signaling are linked to alterations in normal cell functions, and lead to unlimited increased proliferation, sustained angiogenesis, invasion and metastasis. Existing data show that ETS proteins control pathways in epithelial cells as well as stromal compartments, and the crosstalk between the two is essential for normal development and cancer. In this review, we have focused on ETS factors with a known contribution in cancer development. Instead of focusing on a prototype, we address cancer associated ETS proteins and have highlighted the diverse mechanisms by which they affect carcinogenesis. Finally, we discuss strategies for ETS factor targeting as a potential means for cancer therapeutics.
Insights
The E26 transformation-specific (ETS) transcription factors are crucial for cell functions, but their deregulation drives cancer development through various mechanisms. Targeting these ETS factors offers potential therapeutic strategies for various cancers.
Area of Science:
- Molecular Biology
- Cancer Biology
- Genetics
Background:
- E26 transformation-specific (ETS) transcription factors regulate critical cellular processes including development, differentiation, proliferation, apoptosis, and tissue remodeling.
- Deregulation of ETS proteins, through overexpression, gene fusions, or RAS/MAPK pathway modulation, disrupts normal cell functions, leading to uncontrolled proliferation, angiogenesis, invasion, and metastasis.
- ETS proteins influence both epithelial and stromal compartments, with essential crosstalk for normal development and cancer progression.
Purpose of the Study:
- To review the diverse mechanisms by which cancer-associated ETS factors contribute to carcinogenesis.
- To highlight the role of ETS proteins in both normal physiology and cancer development.
- To discuss potential therapeutic strategies targeting ETS factors for cancer treatment.
Main Methods:
- Literature review focusing on ETS factors implicated in cancer development.
- Analysis of mechanisms of ETS protein deregulation and their downstream effects.
- Synthesis of information on ETS protein involvement in epithelial-stromal interactions.
Main Results:
- ETS protein deregulation is linked to key hallmarks of cancer, including sustained proliferation and metastasis.
- ETS factors play diverse roles in carcinogenesis, affecting multiple cellular pathways.
- Targeting ETS factors presents a promising avenue for novel cancer therapeutics.
Conclusions:
- ETS transcription factors are pivotal in cancer development, acting through varied mechanisms.
- Understanding the complex roles of ETS proteins in cancer is crucial for therapeutic development.
- Targeting ETS factors represents a viable strategy for future cancer therapies.
Related Concept Videos
Mitogens and the Cell Cycle
Cancer-Critical Genes I: Proto-oncogenes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Abnormal Proliferation
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Mechanisms of Retrovirus-induced Cancers

