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miR-155 Affects Osteosarcoma MG-63 Cell Autophagy Induced by Adriamycin Through Regulating PTEN-PI3K/AKT/mTOR Signaling Pathway



miR-155 Affects Osteosarcoma MG-63 Cell Autophagy Induced by Adriamycin Through Regulating PTEN-PI3K/AKT/mTOR Signaling Pathway



Cancer BioTherapy and Radiopharmaceuticals 33(1): 32-38



Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) plays a positive regulatory role on cell autophagy through inhibiting PI3K/AKT/mammalian target of rapamycin (mTOR) signaling pathway. miR-155 plays a critical role in osteosarcoma occurrence and chemoresistance. Bioinformatics analysis revealed the targeted binding site between miR-155 and the 3'-UTR (untranslated region) of PTEN mRNA. This study investigated the role of miR-155 in regulating osteosarcoma cell autophagy, chemosensitivity to Adriamycin (ADM), and PTEN-PI3K/AKT/mTOR signaling pathway. Dual luciferase reporter gene assay confirmed the relationship between miR-155 and PTEN. MG-63 cells and drug-resistant MG-63/ADM cells were treated by ADM to compare miR-155, PTEN, p-AKT, p-mTOR, and Beclin-1 expressions. Cell apoptosis was tested by flow cytometry. MG-63/ADM cells were divided into five groups, including anti-miR-NC, anti-miR-155, pSicoR-blank, pSicoR-PTEN, and anti-miR-155+pSicoR-PTEN group. miR-155 targeted suppressed PTEN expression. miR-155, p-AKT, and p-mTOR significantly increased, while PTEN and Beclin-1 obviously reduced in MG-63/ADM cells compared with MG-63 cells. ADM treatment markedly elevated miR-155, p-AKT, and p-mTOR expressions, whereas reduced PTEN level. Beclin-1 was slightly upregulated, and autophagy and apoptosis levels were low. Anti-miR-155 and/or pSicoR-PTEN significantly enhanced PTEN and Beclin-1 expressions, cell apoptosis, and autophagy induced by ADM and declined p-AKT and p-mTOR levels. miR-155 targeted suppressed PTEN expression, enhanced PI3K/AKT/mTOR signaling pathway, inhibited cell apoptosis and autophagy induced by ADM, and reduced sensitivity to ADM.

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Accession: 065321111

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PMID: 29412697

DOI: 10.1089/cbr.2017.2306


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