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MicroRNA 342 is a short, non-coding RNA (20-24 nucleotides) encoded within an intron of the EVL (Ena-vasodilation-stimulating phosphoprotein) gene[1][5][6]. It acts as a post-transcriptional regulator by binding to complementary sequences on target mRNAs, leading to translational inhibition or degradation of those transcripts[1]. MIR342 displays context-dependent roles as either a tumor suppressor or onco-miRNA across multiple cancer types, including breast, colorectal, hepatocellular, nasopharyngeal, and myeloid leukemia, often by targeting oncogenic drivers such as CCND1, BCR-ABL, and Cdc42[2][5][6]. Additionally, it modulates hematopoietic differentiation, angiogenesis in tumors, neural activity, and metabolic processes[3][4]. MIR342's altered expression is associated with various diseases and can predict or influence response to therapies, serving as a diagnostic and prognostic biomarker, with most therapeutic approaches aiming to restore or inhibit its function in malignances or metabolic disorders[5][6].
Sensitization to tyrosine kinase inhibitors (imatinib) by downregulating BCR-ABL expression; Impacting hormone therapy resistance (tamoxifen) by targeting estrogen pathway-related transcripts; Direct targeting of oncogenes and cell cycle regulators: CCND1 (Cyclin D1, cell cycle progression), BCR-ABL (oncogene in CML), Cdc42 (cell division and motility), DNMT1 (epigenetic regulation), AGR2, AEG-1, Ikk-g, TAB2, TAB3, FOXM1, TIAM1 (various cancer-related genes), CXCL12 (chemokine in tumor growth and angiogenesis).
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