Exosomes Derived from Hydroquinone-transformed Human Bronchial Epithelial Cells Inhibited Recipient Cell Apoptosis by transferring miR-221.
- Author:
Hong Yi XIAN
1
;
Ying CHEN
1
;
Jia Ying ZHANG
2
;
Mei Lin TANG
1
;
Zhen Wei LIAN
1
;
Ran JIANG
1
;
Zu Qing HU
3
,
4
;
Yan Feng LI
1
;
Da Lin HU
1
Author Information
- Publication Type:Journal Article
- Keywords: Apoptosis; Benzene; Exosomes; Intercellular communications; Toxic mechanism; miR-221
- MeSH: Apoptosis; Bronchi/cytology*; Cell Line, Transformed; Epithelial Cells; Exosomes; Humans; Hydroquinones; MicroRNAs
- From: Biomedical and Environmental Sciences 2021;34(7):520-527
- CountryChina
- Language:English
-
Abstract:
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 (16HBE-t) and analyzed the level of miR-221 in it with qRT-PCR. Exosomes from 16HBE-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 16HBE 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 16HBE-t was significantly increased compared with controls. When recipient cells ingested exosomes derived from 16HBE-t, miR-221 was increased, and apoptosis induced by HQ was inhibited. Blocking miR-221 in 16HBE-t using an inhibitor did not significantly alter miR-221 or apoptosis in recipient cells.
Conclusion:Exosomal miR-221 secreted by 16HBE-t inhibits apoptosis induced by HQ in normal recipient cells.
