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MicroRNA 302d (miR-302d) is a small, non-coding regulatory RNA molecule encoded by the MIR302D gene located at 4q25 and is a member of the highly conserved miR-302/367 cluster[1][3][5]. miR-302d, like other microRNAs, primarily regulates gene expression by binding to complementary sequences in the 3′-untranslated region (3′-UTR) of target mRNA, leading to translational repression or degradation[1][5]. It is highly expressed in embryonic stem cells and early embryogenesis, where it maintains self-renewal and pluripotency[1][3]. miR-302d regulates the G1/S cell cycle checkpoint, promotes cell proliferation, represses apoptosis, and participates in differentiation and dedifferentiation processes in various cell types[1][3]. In cancer, including hepatocellular carcinoma and testicular germ cell tumors, miR-302d is often upregulated and associated with tumor growth and poor prognosis, in part by targeting pathways such as TGF-beta signaling by repressing tumor suppressor TGFBR2[3][4]. It also modulates key signaling pathways including Hippo and ERK in stem and carcinoma cells[5][7]. The precise functional outcomes of miR-302d modulation are context-dependent and may vary between promoting proliferation in stem cells and oncogenicity in tumor types versus other physiological states[1][3].
Post-transcriptional repression of target mRNAs (e.g., TGFBR2); Regulation of cell cycle pathway proteins; Regulation of signaling pathways (e.g., Hippo, ERK); Other.
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