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Aluminum-maltolate (Al‑Malt) is a potent apoptosis inductor, which has been widely reported as an etiologic factor in Alzheimer's disease (AD). MicroRNA-322 (miR‑322) is a vital regulator in various biological processes. The aim of the current study was to identify the role and possible underlying mechanism of miR‑322 in Al‑Malt‑induced apoptosis. Eight concentrations of Al‑Malt were prepared and used for treating the human neuroblastoma cell line, SH‑SY5Y. Subsequent to treatment with Al‑Malt for 3 days, cell viability, apoptosis and the expression levels of apoptosis‑associated factors were measured. In addition, the mRNA expression level of miR‑322 was monitored. Furthermore, cells were transfected with an miR‑322 mimic and/or treated with Al‑Malt, and cell viability, apoptosis and the expression levels of apoptosis‑associated factors were measured again. Al‑Malt significantly inhibited cell viability, but promoted apoptosis. The apoptosis‑associated factors, V‑Myc avian myelocytomatosis viral oncogene homolog (c‑Myc), Bcl-2-associated X protein, caspase‑3 and cleaved caspase‑3 were markedly upregulated by Al‑Malt. The mRNA expression level of miR‑322 was negatively regulated by Al‑Malt. Furthermore, miR‑322 attenuated the apoptosis induced by Al‑Malt and recovered the expression changes of these four factors. Thus, miR‑322 may attenuate Al‑Malt‑induced apoptosis by recovering the expression change of c‑Myc. Furthermore, miR‑322 may be involved in the pathogenesis of Al‑Malt‑associated AD.

MicroRNA-322 attenuates aluminum maltolate-induced apoptosis in the human SH-SY5Y neuroblastoma cell line