Ascertaining double-strand break repair expression post-REV1 inhibition in IR-exposed cells
Lamkin, Erica N
Lamkin, Erica N
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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.
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Undergraduate
Date
2022-01-01