Abstract
Base excision DNA repair and cancer.
Highlights
The base excision DNA repair (BER) pathway handles simple alkylation and oxidative lesions arising from both endogenous and exogenous sources, including cancer therapy agents
We discovered a function of Ape1 in rRNA metabolism involving direct rRNA binding and interaction with NPM1, which is required for retaining Ape1 in the nucleolus
A role in rRNA metabolism may explain the altered Ape1 expression observed in different tumors [3]
Summary
The base excision DNA repair (BER) pathway handles simple alkylation and oxidative lesions arising from both endogenous and exogenous sources, including cancer therapy agents. Cancer-associated Ape1 variants are often altered in the protein’s DNA repair domain, with some exhibiting nuclease defects in vitro [4]. Up-regulation of Ape1 correlates with the onset of chemoresistance in ovarian, hepatic and neurologic tumors, while inhibition of the protein with small compounds, or the downregulation of its expression, sensitizes cells to DNA-damaging chemotherapeutic drugs and ionizing radiation [3]. Which Ape1 activity is involved in cancer development or chemoresistance remains unknown.
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