Novel REV7 Inhibitors Radiosensitive Cancer Cells
Heney, Seamus
Heney, Seamus
Citations
Altmetric:
License
License
Abstract
Cancer resistance to therapy remains the most challenging aspect of treatment and cure. Dysfunction in several critical cellular pathways causes resistance to chemotherapeutics, with increased mutation formation as a common underlying feature. One major pathway that enhances mutagenesis in cancer cells is Translesion Synthesis (TLS). The formation of the low-fidelity TLS polymerase Pol ?4 depends on REV7, whose dimerization is essential for both its activity and the formation of the Shieldin complex, which links TLS to DNA repair processes. Besides its role in the TLS pathway as an extender past DNA damage, Pol ?4 plays a significant role in determining DNA double-strand break repair choice in the cell, including regulation of the cell cycle and telomere stability. The Shieldin complex orchestrates the selection of the double-strand break repair pathway. Targeting TLS polymerase activity was shown to sensitize cancer cells to DNA-damaging therapies (Chatterjee et al. 2020). In this study, a small molecule inhibitor of REV7 sensitized cancer cells to Ionizing Radiation (IR) in a REV7-dependent manner while inducing autophagy. Collectively, we report the discovery of a novel REV7 inhibitor that radiosensitizes cancer cells while engaging the autophagy mechanism.
Description
Date
1/1/2026
Student Status
Senior (Graduating in 2026)
Journal Title
Journal ISSN
Volume Title
Type of presentation
Poster
Collections
Research Projects
Organizational Units
Journal Issue
Citation
DOI
Advisor(s)
Department
Program/Major
Biological science
College/School
College of Arts and Sciences
Organization
Research Category
Life Science