Exosomes Derived from Hydroquinone-transformed Human Bronchial Epithelial Cells Inhibited Recipient Cell Apoptosis by transferring miR-221

Objective Although benzene is a confirmed environmental carcinogen,the mechanism of its carcinogenicity remains largely unclear.The suggested oncogene,miR-221,is elevated and plays important roles in various tumors,but its role in benzene-induced carcinogenesis remains unknown.Methods In the present study,we constructed hydroquinone(HQ,a representative metabolite of benzene with biological activity)-transformed malignant cell line(16 HBE-t)and analyzed the level of miR-221 in it with qRT-PCR.Exosomes from 16 HBE-t cells incubated with or without an miR-221 inhibitor were isolated by ultracentrifugation,characterized by transmission electron microscopy and laser scanning confocal microscope,and then transfected into 16 HBE cells.The effects of exosomal miR-221 on apoptosis induced by HQ in recipient cells were determined using flow cytometry.Results The amount of miR-221 in 16 HBE-t was significantly increased compared with controls.When recipient cells ingested exosomes derived from 16 HBE-t,miR-221 was increased,and apoptosis induced by HQ was inhibited.Blocking miR-221 in 16 HBE-t using an inhibitor did not significantly alter miR-221 or apoptosis in recipient cells.Conclusion Exosomal miR-221 secreted by 16 HBE-t inhibits apoptosis induced by HQ in normal recipient cells.