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Updated: Aug 6, 2025

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
Published on: June 27, 2020
Role of E2F transcription factor in oral cancer: Recent insight and advancements
Amal Kassab1, Ishita Gupta2, Ala-Eddin Al Moustafa3
1Department of Biomedical Engineering, Faculty of Medicine, McGill University, 3775 University Street, Montreal, QC H3A 2BA, Canada.
Abstract:
The family of mammalian E2F transcription factors (E2Fs) comprise of 8 members (E2F1-E2F8) classified as activators (E2F1-E2F3) and repressors (E2F4-E2F8) primarily regulating the expression of several genes related to cell proliferation, apoptosis and differentiation, mainly in a cell cycle-dependent manner. E2F activity is frequently controlled via the retinoblastoma protein (pRb), cyclins, p53 and the ubiquitin-proteasome pathway. Additionally, genetic or epigenetic changes result in the deregulation of E2F family genes expression altering S phase entry and apoptosis, an important hallmark for the onset and development of cancer. Although studies reveal E2Fs to be involved in several human malignancies, the mechanisms underlying the role of E2Fs in oral cancer lies nascent and needs further investigations. This review focuses on the role of E2Fs in oral cancer and the etiological factors regulating E2Fs activity, which in turn transcriptionally control the expression of their target genes, thus contributing to cell proliferation, metastasis, and drug/therapy resistance. Further, we will discuss therapeutic strategies for E2Fs, which may prevent oral tumor growth, metastasis, and drug resistance.
Insights
Mammalian E2F transcription factors (E2Fs) regulate cell growth and are implicated in cancer. This review explores E2F roles in oral cancer, focusing on therapeutic strategies to combat tumor progression and drug resistance.
Area of Science:
- Molecular Biology
- Genetics
- Oncology
Background:
- E2F transcription factors (E2Fs) are key regulators of cell cycle, proliferation, apoptosis, and differentiation.
- E2F activity is modulated by proteins like pRb, cyclins, p53, and the ubiquitin-proteasome system.
- Deregulation of E2F genes is linked to cancer development by altering cell cycle control and apoptosis.
Purpose of the Study:
- To review the current understanding of E2F family roles in oral cancer.
- To investigate etiological factors influencing E2F activity in oral malignancies.
- To discuss potential therapeutic strategies targeting E2Fs for oral cancer treatment.
Main Methods:
- Literature review of studies on E2Fs in cancer, with a focus on oral cancer.
- Analysis of mechanisms controlling E2F activity and target gene expression.
- Exploration of therapeutic interventions targeting E2F pathways.
Main Results:
- E2Fs play a significant role in oral cancer proliferation, metastasis, and drug resistance.
- Dysregulation of E2F genes is a hallmark of oral tumor development.
- Etiological factors influencing E2F activity in oral cancer require further elucidation.
Conclusions:
- E2Fs are crucial in oral cancer pathogenesis and represent potential therapeutic targets.
- Further research is needed to fully understand E2F mechanisms in oral cancer.
- Targeting E2F pathways may offer novel strategies to prevent oral tumor growth and resistance.
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