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• W4239274327 abstract "Abstract Background: MicroRNAs are non-coding small RNAs that modulate protein expression and implicated in the pathogenesis of much kind of cancers, including multiple myeloma (MM). Previous study revealed that mic-137 was significant down regulated in MM patients compared with health donors. The purpose of this study is to investigate how miR-137 involved in pathogenesis and drug resistance in MM and its potential as prognostic biomarker. Materials and Methods: Real-time RT-PCR was performed to identify the expression of miR-137 in 6 MM cell lines and CD138+ cell sorted from 21 MM patients and 10 healthy donors. The methylation status of miR-137 CpG island was determined by bisulfite pyrosequencing, methylation specific polymerase chain reaction （MSP）and bisulfite sequencing PCR (BSP). The functional roles of miR-137 in MM were characterized by CCK-8 assay, soft agar clonogenic- formation, standard apoptosis assay and CGH array (CytoScanHD Array, Affymetrix). Effect of miR-137 on MM progression in vivo was assessed in the NOD/SCID mice models. In addition, to further identify miR-137 targets, we used bioinformatics analysis and confirmed by luciferase reporter assay. In addition, a total of 19 paired sequential samples with GEP and clinical data, obtained from published studies, were analyzed. Results: The expression of miR-137 was down regulated in all 6 MM cell lines and MM patients (p=0.0017). Further study revealed that methylation of the miR-137 CpG islands was frequently observed in MM cell lines (p<0.0001) and patients (p=0.004) compared with healthy donor by MSP and BSP. Functional study of Cck-8 assay, soft agar clonogenic assay and standard apoptosis assay showed miR-137-OE NCI-H929 significantly inhibited cell proliferation and increased cell drug sensitivity compared with NCI-H929-EV in vitro. Meanwhile, the tumorigenicity of miR-137 overexpressed NCI-H929 reduces tumor volume in xenograft models at day 20 and prolonged the survival of NOD-SCID mice following tail vein injection of miR-137-OE NCI-H929 compared with control (p=0.0198). Overexpression of miR-137 inactivates both AKT and MAPK/ERK Signaling pathway by up-regulating p53 and down-regulating pAKT. Interestingly, CGH-array analysis indicated miR-137 overexpression could decrease chromosomal instability in NCI-H929, such as gain at 1q21, loss at 12p13.31 and 14q22.2 etc. To explore the mechanism of miR-137 involved in chromosome instability, our results demonstrated miR-137 mainly through up regulated AURKA expression and luciferase assay confirmed miR-137 targeted at position 374-380 of AURKA 3’UTR. Conclusion: Our data suggested that miR-137 was epigenetic silenced and targeted AURKA expression to contribute to drug susceptibility and chromosomal Instability in MM. Future studies will be performed on how miR-137 targets AURKA linked to the p53 pathway and evaluating miR-137 as prognostic biomarkers and targets for treatment in MM. Disclosures No relevant conflicts of interest to declare." @default.
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• W4239274327 date "2014-12-06" @default.
• W4239274327 modified "2023-10-18" @default.
• W4239274327 title "MiR-137 Contributes to Drug Susceptibility and Chromosomal Instability of Multiple Myeloma through Targeting AURKA" @default.
• W4239274327 doi "https://doi.org/10.1182/blood.v124.21.5715.5715" @default.
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