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

Abstract

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.