DNA helicases, known for their fundamentally important roles in
genomic stability, are high profile players in
cancer. Not only are there monogenic helicase disorders with a strong disposition to
cancer, it is well appreciated that helicase variants are associated with specific
cancers (e.g.,
breast cancer). Flipping the coin,
DNA helicases are frequently overexpressed in cancerous tissues and reduction in helicase gene expression results in reduced proliferation and growth capacity, as well as DNA damage induction and apoptosis of
cancer cells. The seminal roles of helicases in the DNA damage and replication stress responses, as well as DNA repair pathways, validate their vital importance in
cancer biology and suggest their potential values as targets in anti-
cancer therapy. In recent years, many laboratories have characterized the specialized roles of helicase to resolve transcription-replication conflicts, maintain telomeres, mediate cell cycle checkpoints, remodel stalled replication forks, and regulate transcription. In vivo models, particularly mice, have been used to interrogate helicase function and serve as a bridge for preclinical studies that may lead to novel therapeutic approaches. In this review, we will summarize our current knowledge of
DNA helicases and their roles in
cancer, emphasizing the latest developments.