2/29/2024 0 Comments Jing dong georgia tech masters![]() These miRNAs regulate cell growth, tissue differentiation, and thus are involved in development and disease during life. Only a small fraction of the biological functions of miRNAs are currently elucidated. MicroRNAs are a class of endogenous, non-coding RNAs with regulatory functions that are about 20 to 25 nucleotides in length. Epigenetic modifications such as DNA methylation and microRNA (miRNAs) expression also play a key role in the pathogenesis and progression of leukemia. It has been well established that occurrence of leukemia is the result of different genetic changes, which ultimately leads to malignant transformation. Despite recent advances in the molecular basis of leukemia and the use of new chemotherapy regimens, the overall outlook of AML remains poor. ![]() The pathogenesis involves the inhibition of cell differentiation, uncontrolled proliferation, abnormal apoptosis and so on. It is characterized by the rapid growth of abnormal white blood cells in the bone marrow, which interferes with the production of normal blood cells. Our results suggest that miR-29c down-regulation may act as an independent prognostic biomarker in AML patients, and miR-29c over-expression can increase the sensitivity of both non-resistant and resistant of leukemic cells to DAC.Īcute myeloid leukemia (AML) is a malignant tumor of myeloid progenitor cells. MiR-29c transfection also promoted apoptosis and decreased the IC 50 of DAC in K562/DAC cells. Although miR-29c demethylation was also observed in DAC-resistant K562 (K562/DAC), miR-29c expression was down-regulated. The demethylation of the miR-29c promoter was associated with its up-regulated expression. MiR-29c overexpression decreased the half maximal inhibitory concentration (IC 50) of DAC in K562, while miR-29c silencing increased the IC 50 of DAC in HEL. Over-expression of miR-29c in K562 treated with DAC inhibited growth, while silencing of miR-29c in HEL promoted growth and inhibited apoptosis. Multivariate analysis confirmed the independent prognostic value of low miR-29c expression in both the whole cohort as well as the cytogenetically normal AML (CN-AML) subset. Patients with low miR-29c expression had a markedly shorter overall survival (OS) than those with high miR-29c expression ( P < 0.001). Low miR-29c expression was frequently observed in patients with poor karyotype and high risk ( P = 0.006 and 0.013, respectively). MiR-29c was significantly down-regulated in AML ( P < 0.001). Flow cytometry was used to detect apoptosis. Cell viability after transfection was detected by cell counting Kit-8 assays. ![]() miR-29c/shRNA-29c were respectively transfected into K562 cells and HEL cells. Real-time quantitative PCR (RQ-PCR) was carried out to detect miR-29c transcript level in 102 de novo AML patients and 25 normal controls. We further analyze the influences of miR-29c to leukemic cells treated with DAC. In addition, decitabine (DAC) has made great progress in the treatment of AML in recent years, but DAC resistance is still common phenomenon and the mechanism of resistance is still unclear. Herein, we investigate the effects of abnormal miR-29c expression and analyze its clinical significance in acute myeloid leukemia (AML) patients. MicroRNA-29c (miR-29c) is abnormally expressed in several cancers and serves as an important predictor of tumor prognosis.
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