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CRK mRNA encodes the CRK proto-oncogene, an adaptor protein that plays a pivotal role in intracellular signal transduction [1, 2]. The resulting protein contains SH2 and SH3 domains, which allow it to bridge tyrosine kinases and downstream effector proteins to regulate cell adhesion, migration, and cytoskeletal organization [3]. In various malignancies, including lung, breast, and ovarian cancers, CRK is frequently overexpressed, contributing to tumor progression, epithelial-mesenchymal transition (EMT), and metastasis [4]. Targeting the CRK mRNA via RNA interference (RNAi) or antisense oligonucleotides (ASOs) is an emerging therapeutic strategy designed to reduce CRK protein levels and inhibit these oncogenic signaling pathways [3, 4]. Research has demonstrated that silencing CRK mRNA can significantly decrease the invasive capacity of cancer cells in vitro and reduce tumor growth in animal models [4]. Additionally, CRK is involved in the cellular entry mechanisms of certain bacterial and viral pathogens, suggesting potential applications for mRNA-targeted therapies in infectious disease [3]. Despite its therapeutic potential, the ubiquitous expression of CRK in normal tissues poses challenges for achieving tissue-specific delivery and avoiding systemic toxicity [4]. Consequently, current development efforts focus on optimizing delivery systems to enhance the precision of CRK mRNA knockdown.
RNA interference or antisense-mediated degradation of mRNA to prevent translation of the CRK adaptor protein.
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