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MicroRNA-98 (miR-98) is a small, non-coding RNA molecule and a prominent member of the let-7 microRNA family, located on the X chromosome (Xp11.22). It plays a vital role in post-transcriptional gene regulation by binding to the 3' UTR of various target mRNAs, thereby controlling the expression of genes involved in cell growth, apoptosis, and metastasis [1, 3]. In the context of disease, miR-98 is most extensively studied in oncology, where it primarily acts as a tumor suppressor by targeting oncogenic drivers such as HMGA2, RAS, and MYC; however, its role can be context-dependent, sometimes acting as an oncomir in specific malignancies [2, 13]. Beyond cancer, miR-98 is implicated in regulating inflammatory cytokines and has been associated with neurodegenerative conditions and cardiovascular stability [9]. From a therapeutic perspective, miR-98 is being explored both as a diagnostic biomarker and a druggable target. Current therapeutic strategies focus on using miR-98 mimics to restore expression in downregulated cancers or inhibitors (antagomirs) to silence its activity when it promotes disease, though these approaches remain largely in the preclinical and early developmental stages due to challenges in targeted delivery and potential off-target effects [10, 15].
MicroRNA-98 functions by binding to the 3' untranslated region (3' UTR) of target messenger RNAs (mRNAs) through sequence complementarity, which leads to mRNA degradation or translational inhibition of target genes such as HMGA2, RAS, and IGF1R.
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