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Mature let-7f microRNA is a member of the highly conserved lethal-7 (let-7) family of microRNAs, which are essential regulators of gene expression across various biological processes (Roush & Slack, 2008, Development). It primarily functions as a tumor suppressor by post-transcriptionally downregulating key oncogenes such as RAS, MYC, and HMGA2 (Johnson et al., 2005, Cell). In many human cancers, including lung, breast, and ovarian malignancies, let-7f expression is significantly reduced, which correlates with poor prognosis and tumor progression (Takamizawa et al., 2004, Cancer Research). Beyond its role in oncology, let-7f is involved in cardiovascular development and the modulation of inflammatory responses (Boyerinas et al., 2010, Cancer Research). Therapeutic approaches targeting let-7f include the use of synthetic microRNA mimics to restore its suppressive function or small molecules that inhibit Lin28, a protein that blocks let-7 maturation (Wang et al., 2015, Cell). Despite its therapeutic potential, challenges such as efficient delivery to target tissues and the risk of off-target effects remain significant hurdles in the development of let-7f-based therapies (Babar et al., 2012, Future Medicinal Chemistry). Additionally, the activation of the innate immune system by exogenous RNA molecules presents a safety concern for clinical application (Babar et al., 2012).
Binds to the 3' untranslated region (UTR) of target mRNAs via seed sequence complementarity, leading to translational inhibition or mRNA cleavage and degradation (Roush & Slack, 2008).
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