Ascertaining double-strand break repair expression post-REV1 inhibition in IR-exposed cells
Conference Year
January 2022
Abstract
Translesion synthesis (TLS), a DNA damage tolerance mechanism, causes cancer resistance to therapy. Recently, we determined that REV1 inhibition fails to sensitize cancer cells to ionizing radiation (IR) and triggers autophagy, a biomarker of radioresistance. IR causes double-strand breaks in recipient cells, which if left unrepaired should trigger cell death. However, REV1 inhibition allows IR-exposed cancer cells to continue to proliferate which suggests that REV1 may differentially regulate double-strand break repair (DSBR) expression in the IR-exposed cells. These observations necessitated that DSBR expression be examined. Here, DSBR expression post-REV1 inhibition in IR-exposed cells is examined through western blotting and qPCR.
Primary Faculty Mentor Name
Nimrat Chatterjee
Graduate Student Mentors
Kanayo Ikeh, Josh Victor
Status
Undergraduate
Student College
College of Agriculture and Life Sciences
Second Student College
Graduate College
Program/Major
Molecular Genetics
Primary Research Category
Biological Sciences
Ascertaining double-strand break repair expression post-REV1 inhibition in IR-exposed cells
Translesion synthesis (TLS), a DNA damage tolerance mechanism, causes cancer resistance to therapy. Recently, we determined that REV1 inhibition fails to sensitize cancer cells to ionizing radiation (IR) and triggers autophagy, a biomarker of radioresistance. IR causes double-strand breaks in recipient cells, which if left unrepaired should trigger cell death. However, REV1 inhibition allows IR-exposed cancer cells to continue to proliferate which suggests that REV1 may differentially regulate double-strand break repair (DSBR) expression in the IR-exposed cells. These observations necessitated that DSBR expression be examined. Here, DSBR expression post-REV1 inhibition in IR-exposed cells is examined through western blotting and qPCR.