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RecQ-like helicase (RECQL), also known as RECQL1, is a member of the highly conserved RecQ family of DNA helicases that are essential for maintaining genomic stability [UniProt: P46063]. It functions as an ATP-dependent enzyme that unwinds double-stranded DNA, playing a critical role in DNA replication, recombination, and multiple DNA repair pathways, including base excision repair and double-strand break repair [PubMed: 28655773]. In human health, RECQL is recognized as a tumor suppressor, and germline mutations in the RECQL gene have been linked to an increased risk of hereditary breast and pancreatic cancers [PubMed: 25944712]. Conversely, because many cancer cells exhibit high levels of replication stress and rely on RECQL for survival, it has emerged as a promising therapeutic target for "synthetic lethality" strategies [PubMed: 26903044]. Current drug development efforts focus on small molecule inhibitors and RNA interference (RNAi) technologies to disrupt RECQL activity, aiming to induce apoptosis specifically in malignant cells while minimizing impact on normal tissues [ClinicalTrials.gov: NCT01158079].
Inhibition of ATP-dependent DNA helicase activity, leading to replication stress, DNA damage accumulation, and apoptosis [PubMed: 28655773].
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