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MicroRNA let-7d-3p is a mature, non-coding RNA molecule belonging to the highly conserved let-7 family, which plays a pivotal role in post-transcriptional gene regulation [2, 4]. It is derived from the 3' arm of the pre-let-7d precursor and functions by binding to the 3' untranslated regions (UTRs) of target mRNAs, leading to their degradation or translational inhibition [1, 10]. This miRNA is involved in critical biological processes including cell proliferation, apoptosis, and the immune response, and its dysregulation is linked to various diseases such as cancer, heart failure, and sepsis [5, 7, 8]. In many malignancies, let-7d-3p acts as a tumor suppressor by targeting oncogenes like HMGA2 and RAS, and its expression levels often correlate with patient response to chemotherapy [1, 5]. Therapeutic strategies targeting let-7d-3p include the use of miRNA mimics to restore its suppressive function or antagomirs to inhibit its activity in conditions where it is pathologically upregulated [4, 6]. As a circulating molecule, it also serves as a promising non-invasive biomarker for the early detection and prognosis of several clinical conditions [9, 11]. However, the therapeutic application of let-7d-3p faces challenges such as off-target effects due to its ability to regulate multiple genes and the need for efficient delivery systems [4, 16]. Its role can also be context-dependent, acting as either a tumor suppressor or an oncogene depending on the specific cellular environment and disease state [2, 5].
RNA interference-mediated post-transcriptional gene silencing through translational repression or mRNA degradation of target genes such as HMGA2, YY1, and RAS [1, 10, 15].
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