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Helicase POLQ-like (HELQ) is an ATP-dependent DNA helicase that plays a key role in DNA repair, especially at stalled replication forks, by unwinding DNA and facilitating homologous recombination and other repair mechanisms[1][2][4][5]. HELQ interacts with DNA repair proteins such as replication protein A (RPA) and RAD51 and is essential for maintaining genome stability, resolving DNA damage, and promoting cell survival following genotoxic stress[1][4][5]. It belongs to the Superfamily II group of helicases and acts with a 3’-5’ polarity[1][2][4]. HELQ deficiency increases sensitivity to DNA crosslinking agents and predisposes individuals to ovarian and pituitary tumors, as well as infertility due to germ cell loss[2][4]. Although not currently directly targeted by drugs, HELQ’s role in repair of therapy-induced DNA damage makes it a potential future cancer therapeutic target, and its mutations have diagnostic and prognostic relevance in ovarian cancer[2][3][4][5].
Not applicable directly; however, chemotherapy agents that cause DNA crosslinks or replication-blocking lesions (e.g., cisplatin, mitomycin C) exert increased cytotoxicity when HELQ function is absent or impaired, because DNA repair processes are compromised[4][5].
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