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Chemosphere. 2019 Nov 27;244:125496. doi: 10.1016/j.chemosphere.2019.125496. [Epub ahead of print]

Exosomes derived from normal human bronchial epithelial cells down-regulate proliferation and migration of hydroquinone-transformed malignant recipient cells via up-regulating PTEN expression.

Author information

1
Department of Environmental Health, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, 510515, China.
2
Department of Environmental Health, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, 510515, China; Department of Medicine, Jiamusi University, Jiamusi, 154007, China.
3
Oregon Institute of Occupational Health Sciences, Oregon Health & Science University, 3181 S. W. Sam Jackson Park Rd, Portland, OR, 97239, USA.
4
Nanshan District Center for Disease Control and Prevention, Shenzhen, 518054, China.
5
Institute of Occupational Disease, Shenzhen Prevention and Treatment Center for Occupational Disease, Shenzhen, 518020, China.
6
Faculty of Health Sciences, University of Macau, Taipa, SAR, Macau, China.
7
Department of Environmental Health, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, 510515, China. Electronic address: smuhdl@126.com.

Abstract

The gene encoding the tumor suppressor, phosphatase and tensin homolog (PTEN), located on chromosome 10, is frequently expressed at low levels in various tumors, resulting in the stimulation of cell proliferation and migration. However, the role of exosomal PTEN in cell-cell communication during the progress of benzene-induced carcinogenesis remains unclear. The goal of this study was to explore whether exosomes derived from normal human bronchial epithelial cells (16HBE) could transmit PTEN to hydroquinone-transformed malignant recipient cells (16HBE-t) and its possible effects on cell proliferation and migration. Consistent with PTEN expression being down-regulated in transformed cells, we found that its expression was significantly decreased in 16HBE-t relative to 16HBE cells and that purified exosomes secreted by 16HBE, up-regulated PTEN levels in recipient 16HBE-t cells. Thus, down-regulating their proliferation and migration. Further, when exosomes derived from 16HBE cells that had been treated with the PTEN inhibitor SF1670, were incubated with recipient 16HBE-t cells, they exhibited decreased PTEN levels, with a corresponding increase in their proliferation and migration. In conclusion, our study demonstrates that exosomes derived from 16HBE cells can down-regulate proliferation and migration of recipient 16HBE-t cells via transferring PTEN.

KEYWORDS:

Benzene; Exosomes; Migration; PTEN; Proliferation; Toxicity

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