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MicroRNA let-7i is a short non-coding RNA molecule (20–24 nucleotides) of the let-7 family, evolutionarily conserved and functioning in post-transcriptional gene regulation. By complexing with the RISC machinery, let-7i binds complementary sequences in target mRNAs, leading to decreased protein synthesis by either inhibiting translation or promoting mRNA decay[1][3]. It acts as a tumor suppressor through inhibition of numerous cell cycle and proliferation-related genes, and modulates stem-cell differentiation, apoptosis, and immune functions[1][2]. Dysregulation or loss of let-7i is associated with chemotherapy resistance and poor outcomes in cancer, particularly in ovarian and breast cancer, and its expression level serves as a biomarker for prognosis and patient selection[2][3]. Therapeutic restoration of let-7i, typically via miRNA mimics or gene therapy, is a developing area in cancer treatment, though off-target effects and delivery difficulties are substantial concerns[2][4]. Let-7i is also implicated in other diseases, including neurodegenerative disorders and inflammation, by virtue of its broad gene regulatory activities[3][1].
miRNA mimicry to restore let-7i function or RNA interference approaches; miRNA inhibition to modulate expression (synthetic inhibitors).
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