LncRNA TRAF3IP2 ‐ AS1 Serves as a Potential Biomarker and Drives Acute Myeloid Leukemia Progression via miR ‐186‐5p/ EP300 Axis

Objective To investigate the expression, clinical significance, and biological function of lncRNA TRAF3IP2‐AS1 in acute myeloid leukemia (AML) and to elucidate its underlying molecular mechanisms. Methods The levels of TRAF3IP2‐AS1, miR‐186‐5p, and EP300 were detected by RT‐qPCR from 132 patients with AML and 130 healthy controls, as well as in AML cell lines. Bioinformatics analysis, dual‐luciferase reporter assays, RIP assays, and other experiments were performed to validate the TRAF3IP2‐AS1/miR‐186‐5p/EP300 regulatory axis. Cell proliferation, apoptosis, and cell cycle were assessed by CCK‐8, flow cytometry, and RT‐qPCR. Results TRAF3IP2‐AS1 was upregulated in AML patient samples and cell lines. TRAF3IP2‐AS1 had good diagnostic efficacy for AML (AUC = 0.909) and was an independent prognostic risk factor for poor prognosis of AML patients. Functional experiments confirmed that silencing TRAF3IP2‐AS1 significantly inhibited AML cell proliferation, induced apoptosis, and caused G1 phase arrest. Mechanistically, TRAF3IP2‐AS1 acted as a ceRNA to sponge miR‐186‐5p, thereby relieving its inhibitory effect on the downstream target gene EP300, and ultimately promoting the malignant biological behavior of AML cells. Conclusion TRAF3IP2‐AS1 promotes AML progression through the miR‐186‐5p/EP300 axis and represents a potential diagnostic biomarker, prognostic indicator, and therapeutic target for AML.