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Dig Liver Dis. 2009 Dec;41(12):875-80. doi: 10.1016/j.dld.2009.04.006. Epub 2009 May 26.

Gastric cancer exosomes promote tumour cell proliferation through PI3K/Akt and MAPK/ERK activation.

Author information

1
Department of Medical Oncology, The First Hospital, China Medical University, NO 155, North Nanjing Street, Heping District, Shenyang City 110001, China.

Abstract

BACKGROUND:

Exosomes are nanometer-sized vesicles that are released by normal and neoplastic cells. Previous studies have focused on the interaction between tumour-derived exosomes and the immune system, as a consequence of immune suppression or enhancement. However, the effects of tumour-derived exosomes on tumour cells themselves have not been well studied.

AIMS:

To investigate the effects of gastric cancer exosomes on tumour cell proliferation and the possible mechanisms.

METHODS:

By serial centrifugation and sucrose gradient ultracentrifugation, we isolated and purified the exosomes from gastric cancer SGC7901 cells, then viewed them by electron microscopy. Cell proliferation was measured by 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide assay. Protein expression was assayed by Western blotting.

RESULTS:

SGC7901-cell-derived exosomes promoted the proliferation of SGC7901 and BGC823 cells. The increase in proliferation induced by exosomes was accompanied by activation of Akt and extracellular-regulated protein kinase, and phosphoinositide 3-kinase or extracellular-regulated protein kinase inhibitor partially reversed the proliferative effect of exosomes. Moreover, the exosome-induced increase in activity of Akt and extracellular-regulated protein kinase coincided with decreased expression of the Casitas B-lineage lymphoma family of ubiquitin ligases.

CONCLUSION:

Gastric cancer exosomes promoted tumour cell proliferation, at least in part, by activation of PI3K/Akt and mitogen-activated protein kinase/extracellular-regulated protein kinase pathways. The decreased expression of Casitas B-lineage lymphoma proteins might have contributed to the activation of Akt and extracellular-regulated protein kinase.

PMID:
19473897
DOI:
10.1016/j.dld.2009.04.006
[Indexed for MEDLINE]

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