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ATP-dependent DNA helicase Q1 (RECQL1) is a member of the RecQ family of helicases, which are critical for maintaining genomic integrity by resolving DNA intermediates during replication, recombination, and repair (UniProt P46063). RECQL1 is frequently upregulated in various cancers, including hepatocellular carcinoma and pancreatic cancer, where it facilitates the survival of rapidly dividing cells by managing replication stress (PubMed: 18429944). Because of its overexpression in tumors compared to normal tissues, RECQL1 mRNA has emerged as a therapeutic target for RNA interference (RNAi) therapies. For instance, ALN-VSP02 is a lipid nanoparticle formulation containing siRNAs targeting both RECQL1 and VEGF, designed to inhibit tumor proliferation and angiogenesis simultaneously (ClinicalTrials.gov: NCT00882180). Silencing RECQL1 leads to the accumulation of DNA damage, cell cycle arrest, and apoptosis in cancer cells, making it a promising target for precision oncology (PubMed: 17254008). Furthermore, germline mutations in the RECQL1 gene have been identified as a susceptibility factor for hereditary breast cancer, highlighting its importance in DNA damage response pathways (PubMed: 25915575).
RNA interference (siRNA) leading to mRNA degradation and subsequent reduction in protein expression, thereby inhibiting DNA repair and inducing apoptosis in cancer cells.
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