期刊
JOURNAL OF APPLIED TOXICOLOGY
卷 40, 期 2, 页码 224-233出版社
WILEY
DOI: 10.1002/jat.3898
关键词
benzene; cell viability; exosomes; intercellular communications; miR-221; toxic mechanism
类别
资金
- Science and Technology Project of Shenzhen city [JCYJ20160428173527959, JCYJ20160427111040009]
- Science and Technology Project of Guangzhou [201803030027]
- Science and Technology Project of Guangdong Province [2014A020212206]
- National Natural Science Foundation of China [21677066]
miR-221, an oncogenic microRNA, can promote cell proliferation and is highly expressed in various types of tumors. However, the role of exosomal miR-221 in benzene-caused carcinogenesis remains elusive. Our study was designed to investigate whether exosomes secreted by the hydroquinone (HQ; an active metabolite of benzene)-transformed malignant cells can transmit miR-221 to normal recipient cells and its possible effects on cell viability. Our investigation revealed that expression levels of miR-221 were significantly increased in HQ-transformed malignant cells relative to normal controls. Furthermore, exposure of control cells to exosomes that were derived from HQ-transformed malignant cells increased miR-221 levels and promoted their proliferation. Analyses of the biological potency of exosomes derived from HQ-transformed malignant cells in which miR-221 levels were decreased using an inhibitor, showed that both miR-221 levels and proliferation of recipient cells were decreased, but still were higher than those of normal 16HBE cells. Our study indicates that exosomal miR-221 derived from HQ-transformed malignant human bronchial epithelial cells is involved in the proliferation of recipient cells.
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