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

PTEN公司 张力素 癌症研究 细胞生长 癌变 微泡 细胞迁移 细胞 生物 细胞生物学 化学 PI3K/AKT/mTOR通路 信号转导 小RNA 基因 生物化学
作者
Zhenwei Lian,Zuqing Hu,Hongyi Xian,Ran Jiang,Haoyu Huang,Yunxia Jiang,Zhongdaixi Zheng,R. Stephen Lloyd,Jianhui Yuan,Yan Sha,Sanming Wang,Dalin Hu
出处
期刊:Chemosphere [Elsevier]
卷期号:244: 125496-125496 被引量:11
标识
DOI:10.1016/j.chemosphere.2019.125496
摘要

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.

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