REV1 inhibition elicits differential response to cancer therapy
Conference Year
2023
Abstract
Developing methods to target resistance mechanisms is an important avenue in cancer research. A DNA damage tolerance pathway, translesion synthesis (TLS), contributes to resistance through bypassing DNA damage caused by genotoxic therapies. TLS inhibition is an emerging area of research, and it has been shown that REV1 inhibition, a TLS polymerase, sensitizes cancer cells to cisplatin treatment. In this study, we address whether REV1 inhibition similarly sensitizes cancer cells to radiation therapy. We found that REV1 inhibition confers radioresistance and triggers autophagy. These findings present REV1 as a modulator of response to cancer therapy and warrants further investigation
Primary Faculty Mentor Name
Nimrat Chatterjee
Graduate Student Mentors
Kanayo Ikeh
Status
Undergraduate
Student College
College of Agriculture and Life Sciences
Second Student College
Patrick Leahy Honors College
Program/Major
Microbiology
Primary Research Category
Life Sciences
REV1 inhibition elicits differential response to cancer therapy
Developing methods to target resistance mechanisms is an important avenue in cancer research. A DNA damage tolerance pathway, translesion synthesis (TLS), contributes to resistance through bypassing DNA damage caused by genotoxic therapies. TLS inhibition is an emerging area of research, and it has been shown that REV1 inhibition, a TLS polymerase, sensitizes cancer cells to cisplatin treatment. In this study, we address whether REV1 inhibition similarly sensitizes cancer cells to radiation therapy. We found that REV1 inhibition confers radioresistance and triggers autophagy. These findings present REV1 as a modulator of response to cancer therapy and warrants further investigation