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Updated: May 20, 2026

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Regulation of oncogene-induced cell cycle exit and senescence by chromatin modifiers
1Department of Pharmacology and NYU Cancer Institute, NYU Langone Medical Center, New York, NY, USA. gregory.david@nyumc.org
Abstract:
Oncogene activation leads to dramatic changes in numerous biological pathways controlling cellular division, and results in the initiation of a transcriptional program that promotes transformation. Conversely, it also triggers an irreversible cell cycle exit called cellular senescence, which allows the organism to counteract the potentially detrimental uncontrolled proliferation of damaged cells. Therefore, a tight transcriptional control is required at the onset of oncogenic signal, coordinating both positive and negative regulation of gene expression. Not surprisingly, numerous chromatin modifiers contribute to the cellular response to oncogenic stress. While these chromatin modifiers were initially thought of as mere mediators of the cellular response to oncogenic stress, recent studies have uncovered a direct and specific regulation of chromatin modifiers by oncogenic signals. We review here the diverse functions of chromatin modifiers in the cellular response to oncogenic stress, and discuss the implications of these findings on the regulation of cell cycle progression and proliferation by activated oncogenes.
Insights
Oncogene activation triggers cell cycle changes and senescence. Chromatin modifiers, once thought passive, are now known to be directly regulated by oncogenes, impacting cell proliferation.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Biology
Background:
- Oncogene activation initiates complex cellular responses, including transformation and cell cycle arrest (senescence).
- Maintaining cellular homeostasis requires precise transcriptional control to balance proliferation and damage response.
- Chromatin modifiers play a crucial role in cellular responses to oncogenic stress.
Purpose of the Study:
- To review the diverse functions of chromatin modifiers in response to oncogenic stress.
- To discuss the direct regulation of chromatin modifiers by oncogenic signals.
- To explore the implications for cell cycle progression and proliferation control.
Main Methods:
- Literature review of recent studies on oncogenes and chromatin modifiers.
- Analysis of transcriptional regulation mechanisms.
- Discussion of experimental evidence linking oncogenic signals to chromatin modifier activity.
Main Results:
- Chromatin modifiers are not merely mediators but are directly and specifically regulated by oncogenic signals.
- These interactions influence the transcriptional programs driving cell transformation and senescence.
- The interplay between oncogenes and chromatin modifiers is critical for regulating cell cycle progression.
Conclusions:
- Activated oncogenes directly impact chromatin modifiers, influencing gene expression.
- This regulation is key to coordinating cell cycle progression and proliferation.
- Understanding these mechanisms offers insights into cancer development and potential therapeutic targets.
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