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MicroRNA 1292 (MIR1292) is a small non-coding RNA molecule, approximately 20–24 nucleotides in length, that belongs to the microRNA family involved in post-transcriptional gene silencing[1]. MIR1292 is transcribed as part of longer primary transcripts by RNA polymerase II, processed into a precursor, and finally matures via the Dicer enzyme. The mature miR-1292 integrates into the RNA-induced silencing complex (RISC), which then binds to complementary sequences in target mRNAs, leading to translational inhibition or degradation of the mRNA[1]. Functionally, miR-1292-5p acts as a tumor suppressor in gastric carcinoma, inhibiting cell proliferation, migration, and invasion primarily by downregulating the proto-oncogene DEK[2]. It is downregulated in gastric carcinoma tissues and cell lines, and its overexpression results in cell cycle arrest in G1 and reduced tumorigenicity in vitro and in animal models[2]. Additionally, altered miR-1292 expression has been observed as a biomarker in malignant pleural mesothelioma and is associated with prognosis in metastatic colorectal carcinoma—highlighting its value for diagnosis, prognosis, and possibly therapy in cancer[2]. There are currently no drugs directly targeting miR-1292, but modulating its levels (using mimics or antagonists) is being explored as a therapeutic strategy in cancer[2].
Modulation of oncogenic gene expression by direct binding to target mRNAs (e.g., DEK proto-oncogene) leading to mRNA destabilization or translational repression
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